[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 5129
1. George TI, Wrede JE, Bangs CD, Cherry AM, Warnke RA, Arber DA: Low-grade B-Cell lymphomas with plasmacytic differentiation lack PAX5 gene rearrangements. J Mol Diagn; 2005 Aug;7(3):346-51
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low-grade B-Cell lymphomas with plasmacytic differentiation lack PAX5 gene rearrangements.
  • The chromosomal translocation t(9;14)(p13;q32) has been reported in association with lymphoplasmacytic lymphoma (LPL).
  • Although this translocation involving the paired homeobox-5 (PAX5) gene at chromosome band 9p13 and the immunoglobulin heavy chain (IgH) gene at 14q32 has been described in approximately 50% of LPL cases, the actual number of cases studied is quite small.
  • Many of the initial cases associated with t(9;14)(p13;q32) were actually low-grade B-cell lymphomas with plasmacytic differentiation other than LPL.
  • Thus, we analyzed a series of low-grade B-cell lymphomas for PAX5 gene rearrangements.
  • We searched records from the Department of Pathology, Stanford University Medical Center for low-grade B-cell lymphomas, with an emphasis on plasmacytic differentiation, that had available paraffin blocks or frozen tissue.
  • We identified 37 cases, including 13 LPL, 18 marginal zone lymphomas (nodal, extranodal, splenic, and alpha-heavy chain disease), and 6 small lymphocytic lymphomas.
  • All cases failed to demonstrate a PAX5 translocation, indicating that t(9;14)(p13;q32) and other PAX5 translocations are uncommon events in low-grade B-cell lymphomas with plasmacytic differentiation.

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 1992 Nov 15;80(10):2594-9 [1384792.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jan;87(2):628-32 [2153959.001]
  • [Cites] Int J Hematol. 1998 Feb;67(2):191-8 [9631587.001]
  • [Cites] Br J Haematol. 1998 Aug;102(3):691-700 [9722295.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3865-78 [9808580.001]
  • [Cites] Cancer Genet Cytogenet. 2001 Aug;129(1):1-9 [11520558.001]
  • [Cites] Am J Clin Pathol. 2001 Oct;116(4):543-9 [11601139.001]
  • [Cites] Am J Clin Pathol. 2001 Dec;116(6):799-801 [11764065.001]
  • [Cites] Am J Pathol. 2002 Jun;160(6):1967-72 [12057901.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2996-3001 [12351413.001]
  • [Cites] Hum Pathol. 2004 Apr;35(4):447-54 [15116325.001]
  • [Cites] Cancer Genet Cytogenet. 1986 Jul;22(3):219-23 [3085916.001]
  • [Cites] Jpn J Cancer Res. 1988 Nov;79(11):1193-200 [2852183.001]
  • [Cites] Oncogene. 1989 May;4(5):653-7 [2498807.001]
  • [Cites] Blood. 1996 Dec 1;88(11):4110-7 [8943844.001]
  • (PMID = 16049306.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA034233; United States / NCI NIH HHS / CA / CA34233
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / DNA Probes; 0 / DNA-Binding Proteins; 0 / PAX5 protein, human; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1867539
  •  go-up   go-down


2. Jiang X, Ren YP, Lv ZR: Ouabain induces cardiac remodeling in rats independent of blood pressure. Acta Pharmacol Sin; 2007 Mar;28(3):344-52
Hazardous Substances Data Bank. OUABAIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • After 4 and 6 weeks, echocardiography were performed, hemodynamic parameters were measured by invasive cardiac catheterization, changes in cardiac ultrastructure were analyzed using transmission electron microscopy, the collagen fraction of the left ventricle was assessed with Picrosirius red stain, and RT-PCR was applied to evaluate the mRNA level of myosin heavy chain-alpha and -beta in the left ventricle.
  • Moreover, the cardiac MHC-beta mRNA was upregulated by ouabain treatment, whereas MHC-alpha mRNA was downregulated.
  • [MeSH-minor] Animals. Echocardiography. Glyceraldehyde-3-Phosphate Dehydrogenases / biosynthesis. Glyceraldehyde-3-Phosphate Dehydrogenases / genetics. Male. Myosin Heavy Chains / biosynthesis. Myosin Heavy Chains / genetics. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17302996.001).
  • [ISSN] 1671-4083
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cardiotonic Agents; 5ACL011P69 / Ouabain; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases; EC 3.6.4.1 / Myosin Heavy Chains
  •  go-up   go-down


3. Sekine H, Shimizu T, Yang J, Kobayashi E, Okano T: Pulsatile myocardial tubes fabricated with cell sheet engineering. Circulation; 2006 Jul 4;114(1 Suppl):I87-93
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS AND RESULTS: Neonatal rat cardiomyocyte sheets were sequentially wrapped around a resected adult rat thoracic aorta and transplanted in place of the abdominal aorta of athymic rats (n=17).
  • Finally, when myocardial tubes used for aortic replacement were compared with grafts implanted in the abdominal cavity (n=7), we observed significantly increased tissue thickness, as well as expression of brain natriuretic peptide, myosin heavy chain-alpha, and myosin heavy chain-beta.
  • [MeSH-major] Aorta, Abdominal / surgery. Myocardial Contraction. Myocardium / cytology. Myocytes, Cardiac / transplantation. Tissue Engineering / methods
  • [MeSH-minor] Animals. Animals, Newborn. Aorta, Thoracic / transplantation. Cell Culture Techniques / instrumentation. Cells, Cultured / transplantation. Electrocardiography. Gene Expression Profiling. Microsurgery. Myosin Heavy Chains / biosynthesis. Myosin Heavy Chains / genetics. Natriuretic Peptide, Brain / biosynthesis. Natriuretic Peptide, Brain / genetics. Organ Culture Techniques. Rats. Rats, Nude. Rats, Wistar. Temperature

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16820651.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bmyo protein, rat; 0 / natriuretic peptide precursor type B, rat; 114471-18-0 / Natriuretic Peptide, Brain; EC 3.6.4.1 / Myosin Heavy Chains
  •  go-up   go-down


Advertisement
4. Liu Z, Takazaki H, Nakazawa Y, Sakato M, Yagi T, Yasunaga T, King SM, Kamiya R: Partially functional outer-arm dynein in a novel Chlamydomonas mutant expressing a truncated gamma heavy chain. Eukaryot Cell; 2008 Jul;7(7):1136-45

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Partially functional outer-arm dynein in a novel Chlamydomonas mutant expressing a truncated gamma heavy chain.
  • The outer dynein arm of Chlamydomonas flagella contains three heavy chains (alpha, beta, and gamma), each of which exhibits motor activity.
  • Here we report the isolation of a novel mutant, oda2-t, whose gamma heavy chain is truncated at about 30% of the sequence.
  • While the previously isolated gamma chain mutant oda2 lacks the entire outer arm, oda2-t retains outer arms that contain alpha and beta heavy chains, suggesting that the N-terminal sequence (corresponding to the tail region) is necessary and sufficient for stable outer-arm assembly.
  • Thin-section electron microscopy and image analysis localize the gamma heavy chain to a basal region of the outer-arm image in the axonemal cross section.
  • The motility of oda2-t is lower than that of the wild type and oda11 (lacking the alpha heavy chain) but higher than that of oda2 and oda4-s7 (lacking the motor domain of the beta heavy chain).
  • Thus, the outer-arm dynein lacking the gamma heavy-chain motor domain is partially functional.
  • The availability of mutants lacking individual heavy chains should greatly facilitate studies on the structure and function of the outer-arm dynein.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Cell Sci. 1978 Oct;33:235-53 [31367.001]
  • [Cites] J Biol Chem. 1979 Jan 10;254(1):187-96 [214440.001]
  • [Cites] J Cell Biol. 1980 Aug;86(2):446-55 [6447155.001]
  • [Cites] Cell. 1982 Jan;28(1):115-24 [6461414.001]
  • [Cites] J Cell Biol. 1982 Dec;95(3):798-815 [6218174.001]
  • [Cites] J Cell Biol. 1983 Mar;96(3):669-78 [6220019.001]
  • [Cites] J Cell Biol. 1983 May;96(5):1480-5 [6221024.001]
  • [Cites] J Cell Biol. 1983 Sep;97(3):902-8 [6224802.001]
  • [Cites] J Biol Chem. 1984 Oct 10;259(19):12072-80 [6237107.001]
  • [Cites] J Mol Biol. 1984 Dec 25;180(4):1083-118 [6241263.001]
  • [Cites] J Cell Biol. 1985 Apr;100(4):1228-34 [3156867.001]
  • [Cites] J Cell Sci. 1985 Mar;74:181-91 [4030906.001]
  • [Cites] Anal Biochem. 1986 Feb 1;152(2):376-85 [3963370.001]
  • [Cites] J Mol Biol. 1987 Apr 5;194(3):481-94 [2957507.001]
  • [Cites] J Cell Biol. 1988 Nov;107(5):1793-7 [2972730.001]
  • [Cites] J Cell Biol. 1988 Nov;107(5):1799-808 [2460468.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8998-9002 [2461560.001]
  • [Cites] J Cell Biol. 1988 Dec;107(6 Pt 1):2253-8 [2974040.001]
  • [Cites] Eur J Biochem. 1990 Apr 30;189(2):441-6 [2140096.001]
  • [Cites] J Cell Biol. 1991 May;113(3):615-22 [1673127.001]
  • [Cites] J Biochem. 1992 Jun;111(6):758-62 [1386849.001]
  • [Cites] J Cell Biol. 1992 Sep;118(5):1189-200 [1387406.001]
  • [Cites] J Cell Biol. 1993 Aug;122(3):653-61 [8335691.001]
  • [Cites] Genetics. 1993 Oct;135(2):375-84 [8244002.001]
  • [Cites] J Cell Sci. 1994 Mar;107 ( Pt 3):497-506 [7516341.001]
  • [Cites] J Cell Biol. 1996 Feb;132(3):359-70 [8636214.001]
  • [Cites] J Cell Sci. 1995 Dec;108 ( Pt 12):3757-64 [8719882.001]
  • [Cites] J Struct Biol. 1996 Jan-Feb;116(1):155-60 [8742738.001]
  • [Cites] J Cell Biol. 1996 Dec;135(6 Pt 2):1853-65 [8991096.001]
  • [Cites] J Cell Biol. 1997 Jun 2;137(5):1081-90 [9166408.001]
  • [Cites] Cell Motil Cytoskeleton. 1997;37(2):120-6 [9186009.001]
  • [Cites] Cell Motil Cytoskeleton. 1997;37(4):338-45 [9258506.001]
  • [Cites] J Cell Sci. 1998 May;111 ( Pt 9):1155-64 [9547292.001]
  • [Cites] Biochemistry. 1999 Jun 1;38(22):7253-64 [10353837.001]
  • [Cites] Mol Biol Cell. 2005 Dec;16(12):5661-74 [16195342.001]
  • [Cites] J Biol Chem. 2005 Dec 16;280(50):41412-20 [16236707.001]
  • [Cites] J Cell Sci. 2006 Aug 15;119(Pt 16):3443-55 [16882690.001]
  • [Cites] Science. 2006 Aug 18;313(5789):944-8 [16917055.001]
  • [Cites] J Cell Biol. 2007 Apr 23;177(2):243-52 [17438074.001]
  • [Cites] J Cell Sci. 2007 May 1;120(Pt 9):1513-20 [17405810.001]
  • [Cites] J Mol Biol. 2007 May 18;368(5):1249-58 [17391698.001]
  • [Cites] Cell Motil Cytoskeleton. 2000 Jul;46(3):190-9 [10913966.001]
  • [Cites] Mol Biol Cell. 2000 Jul;11(7):2297-313 [10888669.001]
  • [Cites] Mol Biol Cell. 2007 Sep;18(9):3620-34 [17634291.001]
  • [Cites] Methods. 2000 Dec;22(4):383-7 [11133244.001]
  • [Cites] Int Rev Cytol. 2002;219:115-55 [12211628.001]
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):43571-9 [12923201.001]
  • [Cites] Cell Motil Cytoskeleton. 2004 Mar;57(3):186-96 [14743351.001]
  • [Cites] J Struct Biol. 2004 Apr-May;146(1-2):58-71 [15037237.001]
  • [Cites] J Biol Chem. 1979 Apr 25;254(8):3091-9 [429335.001]
  • (PMID = 18487347.001).
  • [ISSN] 1535-9786
  • [Journal-full-title] Eukaryotic cell
  • [ISO-abbreviation] Eukaryotic Cell
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM051293; United States / NIGMS NIH HHS / GM / GM51293
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Subunits; 0 / Protozoan Proteins; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.4.2 / Dyneins
  • [Other-IDs] NLM/ PMC2446680
  •  go-up   go-down


5. Economidou I, Manousos ON, Triantafillidis JK, Vaslamatzis MM, Zafiropoulou R, Papadakis T: Immunoproliferative small intestinal disease in Greece: presentation of 13 cases including two from Albania. Eur J Gastroenterol Hepatol; 2006 Sep;18(9):1029-38
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoproliferative small intestinal disease in Greece: presentation of 13 cases including two from Albania.
  • OBJECTIVES: Immunoproliferative small intestinal disease (IPSID) represents a spectrum of clinicopathological entities including alpha-chain disease and other types of lymphoplasmacytic proliferations of the lamina propria of the small intestine, presenting with severe malabsorption.
  • IPSID has been described mainly in the Mediterranean, Middle East, and African countries.
  • METHODS: Current immunological and immunohistochemical methods for the detection of alpha heavy chains and the presence of clonality have been used to study 13 cases of IPSID diagnosed in Greece, two of whom were Albanian residents.
  • RESULTS: The patients were categorized in three subgroups of IPSID: alpha-chain disease (n=8), non-alpha chain disease with other monoclonal immunoglobulins (n=3), and polyclonal 'non-malignant' IPSID (n=2).
  • In several patients the disease had unusual features, and this in some cases delayed the diagnosis.
  • Patients with stage C disease had a short survival, whereas two patients with stage A alpha-chain disease responded to treatment with cyclophosphamide, vincristine and prednisolone, and cyclophosphamide, doxorubicine, vincristine and prednisolone, respectively, have a disease-free long survival of 35 and 12 years, and appear to be cured.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / diagnosis

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16894320.001).
  • [ISSN] 0954-691X
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone
  •  go-up   go-down


6. Hara T, Tsurumi H, Kato T, Imao Y, Kojima Y, Kojima K, Kitagawa J, Katsumura N, Araki H, Takami T, Moriwaki H: Immunoproliferative small intestinal disease with protein loss complicated with duodenal T cell lymphoma during progression. Intern Med; 2008;47(4):299-303
MedlinePlus Health Information. consumer health - Intestinal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoproliferative small intestinal disease with protein loss complicated with duodenal T cell lymphoma during progression.
  • A 52-year-old man was admitted to our hospital in October 2001 with abdominal pain.
  • Abdominal X-ray indicated a diagnosis of ileus.
  • Histopathological and immunological examination resulted in a diagnosis of immunoproliferative small intestinal disease (IPSID).
  • He was diagnosed with relapsed IPSID and salvage chemotherapy was started.
  • Immunohistochemical staining revealed T-cell lymphoma.
  • [MeSH-major] Duodenal Neoplasms / etiology. Immunoproliferative Small Intestinal Disease / complications. Lymphoma, T-Cell / etiology
  • [MeSH-minor] Disease Progression. Fatal Outcome. Humans. Male. Middle Aged. Proteins / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18277034.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Proteins
  •  go-up   go-down


7. Vaiphei K, Kumari N, Sinha SK, Dutta U, Nagi B, Joshi K, Singh K: Roles of syndecan-1, bcl6 and p53 in diagnosis and prognostication of immunoproliferative small intestinal disease. World J Gastroenterol; 2006 Jun 14;12(22):3602-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Roles of syndecan-1, bcl6 and p53 in diagnosis and prognostication of immunoproliferative small intestinal disease.
  • AIM: To evaluate roles of syndecan-1, bcl6 and p53 in diagnosis and prognostication of immunoproliferative small intestinal disease (IPSID) and to study profiles of kappa (kappa) and lambda (lambda) light chains and IgA heavy chain.
  • METHODS: The study consisted of 11 cases of IPSID and similar number of controls which included 11 of normal intestinal mucosa and 11 of high grade B cell lymphoma of ileum.
  • The parameters analyzed included clinical profiles, biochemical and other laboratory investigations, radiologic and histological findings including immunohistochemistry.
  • RESULTS: All IPSID cases had demonstrable serum IgA heavy chain and heavy mucosal plasma cell infiltration.
  • According to Galian's histological staging, there were 4 patients with stage A and 7 with stage B. kappa and lambda light chains were over-expressed in 7 patients; 1 stage A patient had H pylori-positive active gastritis and eradication of H pylori led to disease remission.
  • Syndecan-1, kappa and lambda light chains and IgA heavy chain showed inverse relationship with bcl6 and p53.
  • CHOP regime was added in 5 patients who developed frank lymphoma.
  • Three died of the disease due to extensive organ infiltration.
  • CONCLUSION: Certain immunomarkers like syndecan-1, kappa and lambda light chains and IgA heavy chain could be of much help in identifying early stage IPSID.
  • Stage B IPSID showed higher expression for bcl6 and p53 than stage A IPSID. bcl6 and p53 expressions correlated with a more advanced disease stage and aggressive tumour behavior.
  • [MeSH-major] DNA-Binding Proteins / genetics. Immunoproliferative Small Intestinal Disease / diagnosis. Immunoproliferative Small Intestinal Disease / genetics. Membrane Glycoproteins / genetics. Proteoglycans / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adult. Anti-Bacterial Agents / therapeutic use. Case-Control Studies. Disease Progression. Doxycycline / therapeutic use. Endoscopy, Gastrointestinal. Female. Gene Expression Regulation. Helicobacter pylori. Humans. Immunoglobulin alpha-Chains / blood. Immunoglobulin alpha-Chains / genetics. Immunoglobulin kappa-Chains / analysis. Immunoglobulin kappa-Chains / genetics. Immunoglobulin lambda-Chains / analysis. Immunoglobulin lambda-Chains / genetics. Immunohistochemistry. Intestinal Mucosa / chemistry. Intestinal Mucosa / microbiology. Intestinal Mucosa / pathology. Intestine, Small / chemistry. Intestine, Small / microbiology. Intestine, Small / pathology. Male. Middle Aged. Prognosis. Syndecan-1. Syndecans

  • Hazardous Substances Data Bank. DOXYCYCLINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hematol Oncol. 2000 Mar;18(1):1-13 [10797525.001]
  • [Cites] Cancer Res. 1994 Mar 1;54(5):1169-74 [8118801.001]
  • [Cites] Trop Gastroenterol. 2001 Jan-Mar;22(1):14-7 [11398237.001]
  • [Cites] Blood. 2003 Jan 15;101(2):706-10 [12393409.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1220-35 [12393483.001]
  • [Cites] Am J Surg Pathol. 2003 Jun;27(6):790-8 [12766583.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1443-8 [12738680.001]
  • [Cites] Indian J Gastroenterol. 1997 Jan;16(1):38 [9167388.001]
  • [Cites] Biochem J. 1997 Oct 1;327 ( Pt 1):1-16 [9355727.001]
  • [Cites] Indian J Gastroenterol. 1998 Jan;17(1):24-7 [9465510.001]
  • [Cites] Blood. 1998 Apr 15;91(8):2679-88 [9531576.001]
  • [Cites] J Gastroenterol Hepatol. 1998 Dec;13(12):1207-11 [9918427.001]
  • [Cites] Hum Pathol. 1999 Apr;30(4):403-11 [10208461.001]
  • [Cites] Am J Gastroenterol. 1999 May;94(5):1139-52 [10235185.001]
  • [Cites] J Clin Invest. 1969 Dec;48(12):2374-89 [4982231.001]
  • [Cites] J Oral Pathol Med. 2003 Oct;32(9):513-21 [12969225.001]
  • [Cites] Science. 1968 Dec 20;162(3860):1396-7 [4177362.001]
  • [Cites] Isr J Med Sci. 1969 Mar-Apr;5(2):151-7 [4184815.001]
  • [Cites] Ann N Y Acad Sci. 1971 Dec 31;190:487-500 [5003015.001]
  • [Cites] Br Med J. 1972 Oct 7;4(5831):47 [4562280.001]
  • [Cites] Gut. 1972 Dec;13(12):947-57 [4119805.001]
  • [Cites] Recent Results Cancer Res. 1972;39:193-9 [4664791.001]
  • [Cites] JAMA. 1974 Aug 19;229(8):1103-4 [4407962.001]
  • [Cites] Br J Cancer Suppl. 1975 Mar;2:356-61 [810152.001]
  • [Cites] Cancer. 1977 May;39(5):2081-101 [404026.001]
  • [Cites] Bull World Health Organ. 1976;54(6):615-24 [829415.001]
  • [Cites] Isr J Med Sci. 1979 Feb;15(2):111-23 [112083.001]
  • [Cites] Br Med J. 1980 Apr 12;280(6220):1043-4 [6773611.001]
  • [Cites] N Engl J Med. 1983 Jun 9;308(23):1401-5 [6405275.001]
  • [Cites] Ann N Y Acad Sci. 1983 Jun 30;409:478-85 [6408973.001]
  • [Cites] J Clin Pathol. 1985 Jun;38(6):601-7 [3159757.001]
  • [Cites] J Clin Pathol. 1987 Nov;40(11):1291-7 [3121678.001]
  • [Cites] Cancer. 1988 Apr 15;61(8):1699-706 [3349430.001]
  • [Cites] Gastroenterology. 1988 Oct;95(4):1106-13 [3410224.001]
  • [Cites] Gastroenterology. 1989 Mar;96(3):750-63 [2914638.001]
  • [Cites] Eur J Cancer Clin Oncol. 1989 May;25(5):851-6 [2472276.001]
  • [Cites] Am J Surg Pathol. 1989 Dec;13(12):1023-33 [2512818.001]
  • [Cites] Cell Regul. 1989 Nov;1(1):27-35 [2519615.001]
  • [Cites] Blood. 1993 Feb 1;81(3):767-74 [8427968.001]
  • [Cites] Hum Pathol. 1993 Jun;24(6):569-70 [8505034.001]
  • [Cites] N Engl J Med. 1994 May 5;330(18):1267-71 [8145781.001]
  • [Cites] Intern Med. 1995 Apr;34(4):255-60 [7606093.001]
  • [Cites] Indian J Gastroenterol. 1996 Oct;15(4):135-41 [8916578.001]
  • [Cites] Indian J Gastroenterol. 1996 Apr;15(2):46-8 [8935933.001]
  • [Cites] Lancet. 1997 Jan 4;349(9044):31-2 [8988128.001]
  • [Cites] Cell. 1997 Feb 7;88(3):323-31 [9039259.001]
  • [Cites] Lancet. 1993 Sep 4;342(8871):575-7 [8102719.001]
  • [Cites] Mol Cell Biol. 1994 Mar;14(3):1815-23 [8114714.001]
  • [Cites] Hum Pathol. 2000 Jul;31(7):871-3 [10923927.001]
  • (PMID = 16773719.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / BCL6 protein, human; 0 / DNA-Binding Proteins; 0 / Immunoglobulin alpha-Chains; 0 / Immunoglobulin kappa-Chains; 0 / Immunoglobulin lambda-Chains; 0 / Membrane Glycoproteins; 0 / Proteoglycans; 0 / SDC1 protein, human; 0 / Syndecan-1; 0 / Syndecans; 0 / Tumor Suppressor Protein p53; N12000U13O / Doxycycline
  • [Other-IDs] NLM/ PMC4087578
  •  go-up   go-down


8. Dillmann W: Cardiac hypertrophy and thyroid hormone signaling. Heart Fail Rev; 2010 Mar;15(2):125-32
Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • These multiple thyroid hormone effects are largely mediated by the action of nuclear based thyroid hormone receptors (TR) the thyroid hormone receptor alpha and beta.
  • Related to myofibrillar proteins, myosin heavy chain alpha is increased by T3 and MHC beta is decreased.
  • [MeSH-minor] Animals. Humans. Myosin Heavy Chains / metabolism. Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism

  • MedlinePlus Health Information. consumer health - Heart Failure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Med. 1996 Nov;101(5):461-7 [8948268.001]
  • [Cites] JAMA. 1996 Mar 6;275(9):687-92 [8594265.001]
  • [Cites] J Mol Cell Cardiol. 1998 May;30(5):923-32 [9618233.001]
  • [Cites] Science. 2007 Apr 27;316(5824):575-9 [17379774.001]
  • [Cites] J Clin Endocrinol Metab. 2007 May;92(5):1736-42 [17327384.001]
  • [Cites] Endocrinology. 2007 Jun;148(6):2870-7 [17317766.001]
  • [Cites] Endocrinology. 2007 Oct;148(10):4786-92 [17628010.001]
  • [Cites] Eur J Endocrinol. 2007 Oct;157(4):515-20 [17893267.001]
  • [Cites] J Mol Cell Cardiol. 2007 Oct;43(4):388-403 [17720186.001]
  • [Cites] J Clin Invest. 2008 Mar;118(3):975-83 [18259611.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Apr;93(4):1351-8 [18171701.001]
  • [Cites] Front Neuroendocrinol. 2008 May;29(2):211-8 [17983645.001]
  • [Cites] Sci Signal. 2008;1(25):pe31 [18577756.001]
  • [Cites] Basic Res Cardiol. 2008 Jul;103(4):308-18 [18274800.001]
  • [Cites] J Am Coll Cardiol. 2008 Sep 30;52(14):1152-9 [18804743.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1425-30 [18784332.001]
  • [Cites] Cardiovasc Pathol. 2009 May-Jun;18(3):183-6 [18402836.001]
  • [Cites] Am J Physiol. 1998 Jul;275(1 Pt 2):H264-73 [9688923.001]
  • [Cites] EMBO J. 1999 Feb 1;18(3):623-31 [9927422.001]
  • [Cites] Am J Physiol. 1999 Jun;276(6 Pt 2):H2006-12 [10362681.001]
  • [Cites] Annu Rev Physiol. 2005;67:69-98 [15709953.001]
  • [Cites] Treat Endocrinol. 2004;3(4):233-44 [16026106.001]
  • [Cites] Endocr Rev. 2005 Aug;26(5):704-28 [15632316.001]
  • [Cites] J Clin Invest. 2005 Aug;115(8):2108-18 [16075055.001]
  • [Cites] Endocrinology. 2005 Nov;146(11):4926-33 [16081636.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2005 Dec;289(6):H2409-15 [16024568.001]
  • [Cites] MedGenMed. 2005;7(1):74 [16369379.001]
  • [Cites] Mol Cell Endocrinol. 2006 Feb 26;246(1-2):121-7 [16442701.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):6043-8 [16595628.001]
  • [Cites] Curr Heart Fail Rep. 2006 Sep;3(3):114-9 [16914103.001]
  • [Cites] J Gen Intern Med. 2007 Jan;22(1):148-50 [17351857.001]
  • [Cites] Physiol Genomics. 2007 Mar 14;29(1):76-83 [17164392.001]
  • [Cites] Heart Fail Clin. 2005 Jul;1(2):207-18 [17386847.001]
  • [Cites] Heart. 2007 Apr;93(4):483-7 [17005710.001]
  • [Cites] Hypertension. 2007 May;49(5):962-70 [17389260.001]
  • [Cites] Cardiovasc Res. 1999 Aug 1;43(2):382-8 [10536668.001]
  • [Cites] J Mol Cell Cardiol. 2000 Mar;32(3):453-64 [10731444.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2000 Apr;278(4):E738-43 [10751209.001]
  • [Cites] Endocrinology. 2000 Jun;141(6):2139-44 [10830301.001]
  • [Cites] N Engl J Med. 2001 Feb 15;344(7):501-9 [11172193.001]
  • [Cites] Endocrinology. 2001 Feb;142(2):544-50 [11159823.001]
  • [Cites] Circulation. 2001 Feb 27;103(8):1089-94 [11222471.001]
  • [Cites] Mol Cell Biol. 2001 Jul;21(14):4761-72 [11416151.001]
  • [Cites] Thyroid. 2002 Apr;12(4):287-93 [12034052.001]
  • [Cites] Endocrinology. 2002 Jul;143(7):2461-5 [12072374.001]
  • [Cites] Endocrinology. 2002 Jul;143(7):2812-5 [12072417.001]
  • [Cites] Thyroid. 2002 Jun;12(6):501-3 [12165113.001]
  • [Cites] Circulation. 2003 Feb 11;107(5):708-13 [12578873.001]
  • [Cites] Endocr Pract. 2003 Mar-Apr;9(2):140-6 [12917077.001]
  • [Cites] Curr Hypertens Rep. 2003 Dec;5(6):513-20 [14594573.001]
  • [Cites] Recent Prog Horm Res. 2004;59:31-50 [14749496.001]
  • [Cites] Mol Cell Endocrinol. 2003 Dec 31;213(1):1-11 [15062569.001]
  • [Cites] Trends Biochem Sci. 2004 Nov;29(11):609-17 [15501680.001]
  • [Cites] Am J Physiol. 1987 Mar;252(3 Pt 2):H467-73 [3826395.001]
  • [Cites] J Biol Chem. 1991 May 5;266(13):8638-46 [1827123.001]
  • [Cites] Circ Res. 1991 Aug;69(2):266-76 [1830516.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5251-5 [1376915.001]
  • [Cites] J Biol Chem. 1995 Jul 7;270(27):16347-54 [7608204.001]
  • [Cites] N Engl J Med. 1995 Dec 7;333(23):1522-7 [7477166.001]
  • [Cites] EMBO J. 1997 Jul 16;16(14):4412-20 [9250685.001]
  • (PMID = 19125327.001).
  • [ISSN] 1573-7322
  • [Journal-full-title] Heart failure reviews
  • [ISO-abbreviation] Heart Fail Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Thyroid Hormone; 0 / Thyroid Hormones; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; EC 3.6.4.1 / Myosin Heavy Chains; SY7Q814VUP / Calcium
  • [Number-of-references] 60
  • [Other-IDs] NLM/ PMC2820695
  •  go-up   go-down


9. Zheng H, Li M, Ren W, Zeng L, Liu HD, Hu D, Deng X, Tang M, Shi Y, Gong J, Cao Y: Expression and secretion of immunoglobulin alpha heavy chain with diverse VDJ recombinations by human epithelial cancer cells. Mol Immunol; 2007 Mar;44(9):2221-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and secretion of immunoglobulin alpha heavy chain with diverse VDJ recombinations by human epithelial cancer cells.
  • Recently, we found the expression of Ig alpha heavy chain in human epithelial cancer cells unexpectedly.
  • Further, the configuration of the Ig heavy chain genomic locus was analyzed in human cancer cells.
  • These provide further proofs for Ig alpha expression.
  • In addition, we found that human cancer cells not only express the protein of Ig alpha chain, but also secrete the protein in secretory IgA (SIgA) pattern.
  • Since IgA is the key immunoglobulin which contributes to local immunity of mucous membrane, the aberrant expression of Ig alpha heavy chain might increase our further comprehension to development and immunity of cancers.
  • [MeSH-major] Epithelial Cells / immunology. Epithelial Cells / pathology. Immunoglobulin A, Secretory / genetics. Immunoglobulin alpha-Chains / genetics. Neoplasms / immunology. Recombination, Genetic. VDJ Exons / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17174398.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Complementarity Determining Regions; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Immunoglobulin A, Secretory; 0 / Immunoglobulin alpha-Chains; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RAG2 protein, human; 0 / RNA, Messenger; 128559-51-3 / RAG-1 protein; EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / Cytidine Deaminase
  •  go-up   go-down


10. Huang YC, Khait L, Birla RK: Modulating the functional performance of bioengineered heart muscle using growth factor stimulation. Ann Biomed Eng; 2008 Aug;36(8):1372-82
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Also, at 25 ng/mL, myosin heavy chain alpha and SERCA2 expression increased by 1.3 +/- 0.188 and 1.1 +/- 0.04 fold, respectively.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18500554.001).
  • [ISSN] 1573-9686
  • [Journal-full-title] Annals of biomedical engineering
  • [ISO-abbreviation] Ann Biomed Eng
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins
  •  go-up   go-down


11. Dutta U, Udawat H, Noor MT, Sidhu GS, Kochhar R, Vaiphei K, Singh K: Regression of immunoproliferative small intestinal disease after eradication of Helicobacter pylori. J Gastrointest Cancer; 2010 Sep;41(3):212-5
Hazardous Substances Data Bank. Clarithromycin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regression of immunoproliferative small intestinal disease after eradication of Helicobacter pylori.
  • A 20-year-old male presented with low-grade fever, abdominal pain, anorexia, and weight loss of 4-month duration.
  • Contrast-enhanced computed tomography of the abdomen revealed extensive proximal small-bowel thickening with mesenteric lymphadenopathy.
  • Upper gastrointestinal endoscopy and enteroscopy revealed thickening of folds with multiple small superficial ulceration involving antrum, duodenum, and jejunum.
  • The duodenal and jejunal biopsy was suggestive of immunoproliferative small intestinal disease, stage 0 (Salem) or stage A (Galian).
  • He underwent H. pylori eradication following which he had significant clinical improvement; repeat evaluation at 6 months showed dramatic improvement in his clinical, radiological, and histological parameters.
  • [MeSH-major] Anti-Bacterial Agents / therapeutic use. Helicobacter Infections / complications. Immunoproliferative Small Intestinal Disease / drug therapy. Immunoproliferative Small Intestinal Disease / microbiology

  • MedlinePlus Health Information. consumer health - Antibiotics.
  • MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.
  • Hazardous Substances Data Bank. TINIDAZOLE .
  • Hazardous Substances Data Bank. AMOXICILLIN .
  • Hazardous Substances Data Bank. DOXYCYCLINE .
  • Hazardous Substances Data Bank. OMEPRAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20300878.001).
  • [ISSN] 1941-6636
  • [Journal-full-title] Journal of gastrointestinal cancer
  • [ISO-abbreviation] J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-Pyridinylmethylsulfinylbenzimidazoles; 0 / Anti-Bacterial Agents; 0 / Organometallic Compounds; 033KF7V46H / Tinidazole; 0K5C5T2QPG / Lansoprazole; 804826J2HU / Amoxicillin; H1250JIK0A / Clarithromycin; HS813P8QPX / bismuth tripotassium dicitrate; KG60484QX9 / Omeprazole; N12000U13O / Doxycycline
  •  go-up   go-down


12. Mielcarek-Kuchta D, Olofsson J, Golusinski W: Laminin expression in advanced laryngeal squamous cell carcinoma does not correlate to neck metastases. Eur Arch Otorhinolaryngol; 2008 Oct;265(10):1257-61
Genetic Alliance. consumer health - Carcinoma, Squamous Cell.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Laminins are a family of glycoproteins that consist of one heavy alpha chain and two light beta and gamma chains.
  • The study was carried out on 70 patients with squamous cell carcinoma of the larynx treated at the ENT Department University of Medical Sciences in Poznań.
  • The clinical data consisted of sex, age, stage of the tumor, and histological and immunohistochemical studies.
  • The patients with advanced clinical disease dominated in our material.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18516614.001).
  • [ISSN] 0937-4477
  • [Journal-full-title] European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
  • [ISO-abbreviation] Eur Arch Otorhinolaryngol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Laminin
  •  go-up   go-down


13. Parfenov AI, Krums LM, Sivash ES, Tsaregorodtseva TM, Poleva NI, Ruchkina IN, Sabel'nikova EA, Chikunova BZ: [Algorithm for diagnosis of small intestinal diseases]. Ter Arkh; 2008;80(4):46-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Algorithm for diagnosis of small intestinal diseases].
  • AIM: To review diagnostic approaches in chronic diseases of the small intestine.
  • MATERIAL AND METHODS: A total of 1096 patients with chronic diseases of the small intestine were admitted to the clinic of the Central Research Institute of Gastroenterological Diseases in 1987-2006.
  • RESULTS: Most of the patients (90.5%) had celiac disease, hypolactasia and other types of disaccharidase deficiency, yersiniosis ileitis, Krohn's disease, postresection syndrome of a short small intestine, mesenterial ischemia and endocrine enteropathy.
  • Rare diseases (general variable hypogammaglobulinemia, lymphoma, Wipple's disease and diverticulosis of the small intestine) were diagnosed in 5.8% cases.
  • Primary amyloidosis of the small intestine, eosinophilic gastroenteritis, arteriomesenterial obstruction, primary intestinal pseudoobstruction, hypogammaglobulinemic spru, primary intestinal lymphangiectasia, tuberculosis, total polyposis, Peutz-Eggers and Cronkhite-Canada syndromes, collagenic sprue, erosive-ulcerative jejunoileitis, adenocarcinoma and heavy alpha-chain disease were detected in 3.7% examinees.
  • These diseases were encountered in one to 5 cases for the latest 20 years.
  • CONCLUSION: Clinical diagnosis of small intestinal diseases is based on the syndromes of chronic diarrhea, defective absorption, enteral protein loss, small intestinal obstruction and intestinal hemorrhage.
  • Differential diagnosis of the nosological entities employs x-ray, endoscopic, histological, immunological and other methods.
  • Most of the small intestinal diseases including rare can be diagnosed in any gastroentorological department.
  • [MeSH-major] Algorithms. Endoscopy, Gastrointestinal / methods. Immunologic Tests / methods. Intestinal Diseases / diagnosis. Intestine, Small. Radiography, Abdominal / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Retrospective Studies

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18491580.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  •  go-up   go-down


14. Ben Ammar A, Cheikh I, Jouini M, Belkahla N, Fadhel SF, Hager O, Maamouri N, Chaabouni H, Ben Safta Z, Haouet S: [Alpha heavy chain disease. A Tunisian case]. Tunis Med; 2006 Sep;84(9):581-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Alpha heavy chain disease. A Tunisian case].
  • [Transliterated title] Maladie des chaines lourdes alpha. A propos d'un cas tunisien.
  • Alpha heavy chain disease is a rare affection in the West and reported mainly in developing countries with the improvement of hygienic conditions, the disease become rare in Tunisia, the last case was reported in 1991.
  • The aim of the study is to report a new Tunisian case and to describe clinical, endoscopical and histological characteristics of the disease.
  • The diagnosis of alpha heavy chain disease was confirmed by histological examination of the resected intestine after surgery for intestinal obstruction.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / diagnosis
  • [MeSH-minor] Adult. Humans. Intestinal Obstruction / etiology. Intestinal Obstruction / surgery. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17263208.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Tunisia
  •  go-up   go-down


15. Zhou H, Hickford JG, Fang Q: Identification of allelic polymorphism in the caprine IGHA gene. Dev Comp Immunol; 2006;30(9):741-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Variation in the immunoglobulin heavy alpha chain (IGHA) constant region has been reported in a number of species.
  • The variation reported here may affect the structure of the hinge and hence the function of IgA.
  • [MeSH-major] Goats / genetics. Goats / immunology. Immunoglobulin alpha-Chains / genetics
  • [MeSH-minor] Alleles. Amino Acid Sequence. Animals. Base Sequence. DNA / chemistry. DNA / genetics. Hinge Exons. Molecular Sequence Data. Polymerase Chain Reaction / veterinary. Polymorphism, Single-Stranded Conformational. Sequence Alignment

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16343618.001).
  • [ISSN] 0145-305X
  • [Journal-full-title] Developmental and comparative immunology
  • [ISO-abbreviation] Dev. Comp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin alpha-Chains; 9007-49-2 / DNA
  •  go-up   go-down


16. Pai RK, Snider WK, Starkey CR, Viswanatha D, Foucar MK, Wilson CS: Nonsecretory variant of immunoproliferative small intestinal disease: a case report with pathologic, immunophenotypic, and molecular findings. Arch Pathol Lab Med; 2005 Nov;129(11):1487-90
Hazardous Substances Data Bank. OMEPRAZOLE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nonsecretory variant of immunoproliferative small intestinal disease: a case report with pathologic, immunophenotypic, and molecular findings.
  • We report a case of the nonsecretory variant of immunoproliferative small intestinal disease involving the distal small bowel and the mesenteric and retroperitoneal lymph nodes in a 19-year-old woman from Mexico.
  • This variant extranodal marginal zone B-cell lymphoma appeared similar in the different sites of involvement, with more interspersed large cells and greater plasmacytic differentiation present in intestinal specimens.
  • Characteristic lymphoepithelial lesions and follicular colonization were seen in intestinal and lymph node sections, respectively.
  • The neoplastic B cells were cytoplasmic immunoglobulin (Ig) A heavy-chain restricted and lacked surface and cytoplasmic light-chain expression by flow cytometric analysis.
  • Molecular studies showed absence of immunoglobulin heavy-chain (IgH) gene rearrangement, with a nonfunctional clonotypic rearrangement of the kappa light-chain gene.
  • This case highlights the role for kappa light-chain gene evaluation in immunoproliferative small intestinal disease, because IgH gene rearrangement analysis is often negative.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / pathology. Lymph Nodes / pathology. Lymphoma, B-Cell, Marginal Zone / pathology
  • [MeSH-minor] 2-Pyridinylmethylsulfinylbenzimidazoles. Adult. Amoxicillin / therapeutic use. Anti-Bacterial Agents / therapeutic use. Benzimidazoles / therapeutic use. Drug Therapy, Combination. Female. Gene Rearrangement, B-Lymphocyte, Light Chain / genetics. Humans. Immunophenotyping. Intestine, Small / pathology. Mesentery. Metronidazole / therapeutic use. Omeprazole / analogs & derivatives. Omeprazole / therapeutic use. Retroperitoneal Space. Sulfoxides / therapeutic use

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PANTOPRAZOLE .
  • Hazardous Substances Data Bank. AMOXICILLIN .
  • Hazardous Substances Data Bank. METRONIDAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16253033.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-Pyridinylmethylsulfinylbenzimidazoles; 0 / Anti-Bacterial Agents; 0 / Benzimidazoles; 0 / Sulfoxides; 140QMO216E / Metronidazole; 804826J2HU / Amoxicillin; D8TST4O562 / pantoprazole; KG60484QX9 / Omeprazole
  •  go-up   go-down


17. Ishikawa T, Sakakibara H, Oiwa K: The architecture of outer dynein arms in situ. J Mol Biol; 2007 May 18;368(5):1249-58

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Outer dynein arms, the force generators for axonemal motion, form arrays on microtubule doublets in situ, although they are bouquet-like complexes with separated heads of multiple heavy chains when isolated in vitro.
  • To understand how the three heavy chains are folded in the array, we reconstructed the detailed 3D structure of outer dynein arms of Chlamydomonas flagella in situ by electron cryo-tomography and single-particle averaging.
  • The three AAA rings of heavy chains, seen as stacked plates, are connected in a striking manner on microtubule doublets.
  • The tail of the alpha-heavy chain, identified by analyzing the oda11 mutant, which lacks alpha-heavy chain, extends from the AAA ring tilted toward the tip of the axoneme and towards the inside of the axoneme at 50 degrees , suggesting a three-dimensional power stroke.
  • The neighboring outer dynein arms are connected through two filamentous structures: one at the exterior of the axoneme and the other through the alpha-tail.
  • Although the beta-tail seems to merge with the alpha-tail at the internal side of the axoneme, the gamma-tail is likely to extend at the exterior of the axoneme and join the AAA ring.
  • This suggests that the fold and function of gamma-heavy chain are different from those of alpha and beta-chains.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17391698.001).
  • [ISSN] 0022-2836
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.6.4.2 / Dyneins
  •  go-up   go-down


18. Zhou H, Hickford JG, Fang Q: Polymorphism of the IGHA gene in sheep. Immunogenetics; 2005 Jul;57(6):453-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study, variation in the immunoglobulin heavy alpha chain constant gene (IGHA) of sheep was investigated by amplification of a fragment that included the hinge coding sequence, followed by single-strand conformational polymorphism (SSCP) analysis and DNA sequencing.
  • [MeSH-major] Immunoglobulin alpha-Chains / genetics. Polymorphism, Single-Stranded Conformational. Sheep / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16025324.001).
  • [ISSN] 0093-7711
  • [Journal-full-title] Immunogenetics
  • [ISO-abbreviation] Immunogenetics
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY956424/ AY956425/ AY956426
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / Immunoglobulin alpha-Chains
  •  go-up   go-down


19. Furuta A, Yagi T, Yanagisawa HA, Higuchi H, Kamiya R: Systematic comparison of in vitro motile properties between Chlamydomonas wild-type and mutant outer arm dyneins each lacking one of the three heavy chains. J Biol Chem; 2009 Feb 27;284(9):5927-35

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systematic comparison of in vitro motile properties between Chlamydomonas wild-type and mutant outer arm dyneins each lacking one of the three heavy chains.
  • Outer arm dynein (OAD) of cilia and flagella contains two or three distinct heavy chains, each having a motor function.
  • To elucidate their functional difference, we compared the in vitro motile properties of Chlamydomonas wild-type OAD containing the alpha, beta, and gamma heavy chains and three kinds of mutant OADs, each lacking one of the three heavy chains.
  • Wild-type OAD displayed microtubule gliding in the presence of ATP and ADP, with a maximal velocity of 5.0 mum/s, which is approximately 1/4 of the microtubule sliding velocity in the axoneme.
  • The absence of the beta heavy chain lowered both the gliding velocity and ATPase activity, whereas the absence of the gamma heavy chain increased both activities.
  • Strikingly, the absence of the alpha heavy chain lowered the gliding velocity but increased the ATPase activity.
  • Thus, the three heavy chains are likely to play distinct roles and regulate each other to achieve coordinated force production.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19124458.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Subunits; EC 3.6.4.2 / Dyneins
  •  go-up   go-down


20. Lin YS, Zhou H, Forrest RH, Frampton CM, Hickford JG: Association between variation in faecal egg count for a mixed field-challenge of nematode parasites and IGHA gene polymorphism. Vet Immunol Immunopathol; 2009 Apr 15;128(4):389-94
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Research has shown that variation in ovine immunoglobulin A (IgA) levels are associated with reduced faecal egg counts (FECs) in sheep hosting gastro-intestinal (GI) parasites.
  • Variation in the constant region of the ovine IgA heavy alpha chain gene (IGHA) may result in structurally and functionally different IgA molecules and may consequently lead to variation in the IgA response to parasitisation.
  • However, when the data was split into predominant challenge type groups, associations were detected.
  • [MeSH-major] Gastrointestinal Diseases / veterinary. Immunoglobulin A / genetics. Nematoda / growth & development. Nematode Infections / veterinary. Sheep Diseases / immunology. Sheep Diseases / parasitology
  • [MeSH-minor] Alleles. Animals. DNA, Helminth / chemistry. DNA, Helminth / genetics. Feces / parasitology. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Heavy Chains / immunology. Male. Parasite Egg Count / veterinary. Polymerase Chain Reaction / veterinary. Polymorphism, Single-Stranded Conformational. Sheep

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19150137.001).
  • [ISSN] 0165-2427
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA, Helminth; 0 / Immunoglobulin A; 0 / Immunoglobulin Heavy Chains
  •  go-up   go-down


21. Quinn BA, Hayes MA, Waelchli RO, Kennedy MW, Betteridge KJ: Changes in major proteins in the embryonic capsule during immobilization (fixation) of the conceptus in the third week of pregnancy in the mare. Reproduction; 2007 Jul;134(1):161-70
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • During fixation, beta2M in the capsule underwent limited proteolysis to an approximately 8 kDa form lacking nine amino acids from the N terminus, and was subsequently degraded.
  • During this period, beta2M in the capsule was evidently not part of a complex with major histocompatibility complex class 1 heavy alpha chain bands because these were undetectable in the capsule and uterine lavage.
  • These studies indicate that intact beta2M is a major protein associated with the embryonic capsule before fixation, after which it undergoes limited proteolysis to a truncated approximately 8 kDa form that remains in the capsule after the conceptus is immobilized.
  • [MeSH-minor] Animals. Electrophoresis, Polyacrylamide Gel. Female. Gene Expression. Gestational Age. Histocompatibility Antigens Class I / genetics. Histocompatibility Antigens Class I / metabolism. Immunoblotting. Pregnancy. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Uteroglobin / analysis. Uteroglobin / metabolism. Uterus / chemistry. Uterus / metabolism. Yolk Sac / chemistry. Yolk Sac / metabolism. beta 2-Microglobulin / analysis. beta 2-Microglobulin / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17641098.001).
  • [ISSN] 1470-1626
  • [Journal-full-title] Reproduction (Cambridge, England)
  • [ISO-abbreviation] Reproduction
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glycoproteins; 0 / Histocompatibility Antigens Class I; 0 / MHC class I-related chain A; 0 / RNA, Messenger; 0 / beta 2-Microglobulin; 9060-09-7 / Uteroglobin
  •  go-up   go-down


22. Lampton PW, Goldstein CY, Warner CM: The role of tapasin in MHC class I protein trafficking in embryos and T cells. J Reprod Immunol; 2008 Jun;78(1):28-39
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Similar in structure to MHC class Ia proteins, Qa-2 protein is a trimer of the alpha (heavy) chain, beta(2) microglobulin and a bound peptide.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Immunity. 1996 Aug;5(2):103-14 [8769474.001]
  • [Cites] J Immunol. 1994 Jun 1;152(11):5268-74 [8189046.001]
  • [Cites] Am J Reprod Immunol. 1998 Sep;40(3):165-71 [9764360.001]
  • [Cites] Mol Hum Reprod. 1998 Oct;4(10):966-71 [9809678.001]
  • [Cites] Reprod Fertil Dev. 2004;16(7):729-41 [15740696.001]
  • [Cites] Immunol Rev. 2005 Oct;207:89-99 [16181329.001]
  • [Cites] Immunol Rev. 2005 Oct;207:145-57 [16181333.001]
  • [Cites] J Cell Sci. 2006 Feb 15;119(Pt 4):615-23 [16467570.001]
  • [Cites] J Physiol. 2006 Feb 15;571(Pt 1):211-20 [16269433.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Oct 31;103(44):16412-7 [17056715.001]
  • [Cites] Hum Immunol. 2007 Jan;68(1):1-11 [17207707.001]
  • [Cites] Biol Reprod. 2007 Aug;77(2):274-9 [17442853.001]
  • [Cites] Transplantation. 1999 Dec 15;68(11):1790-9 [10609958.001]
  • [Cites] J Reprod Immunol. 2000 Feb;46(1):1-15 [10708239.001]
  • [Cites] Immunity. 2000 Aug;13(2):213-22 [10981964.001]
  • [Cites] Cancer Res. 2001 Feb 1;61(3):1095-9 [11221838.001]
  • [Cites] Nat Immunol. 2000 Sep;1(3):234-8 [10973281.001]
  • [Cites] Trends Immunol. 2001 Apr;22(4):194-9 [11274924.001]
  • [Cites] Curr Top Dev Biol. 2001;52:151-92 [11529429.001]
  • [Cites] Immunogenetics. 2001 Aug;53(6):455-67 [11685456.001]
  • [Cites] Structure. 2001 Dec;9(12):1213-24 [11738047.001]
  • [Cites] J Immunol. 2002 Mar 1;168(5):2200-11 [11859106.001]
  • [Cites] Immunity. 2002 Apr;16(4):509-20 [11970875.001]
  • [Cites] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886.001]
  • [Cites] Hum Reprod. 2002 Nov;17(11):2938-47 [12407053.001]
  • [Cites] Nature. 2002 Dec 5;420(6915):520-62 [12466850.001]
  • [Cites] J Immunol. 2003 Jan 15;170(2):961-8 [12517962.001]
  • [Cites] Annu Rev Immunol. 2003;21:629-57 [12500978.001]
  • [Cites] J Biol Chem. 2003 Apr 18;278(16):14337-45 [12582157.001]
  • [Cites] J Immunol. 2003 May 1;170(9):4515-23 [12707328.001]
  • [Cites] Nucleic Acids Res. 2003 Dec 15;31(24):e154 [14654707.001]
  • [Cites] Reprod Biol Endocrinol. 2003 Feb 14;1:27 [12646049.001]
  • [Cites] J Immunol. 2004 Oct 1;173(7):4394-401 [15383569.001]
  • [Cites] Biol Reprod. 1987 Apr;36(3):611-6 [3593833.001]
  • [Cites] J Reprod Immunol. 1991 Apr;19(3):303-13 [1865393.001]
  • [Cites] Nature. 1992 Feb 13;355(6361):644-6 [1538752.001]
  • [Cites] Nature. 1993 Feb 18;361(6413):642-4 [8437623.001]
  • [Cites] Biol Reprod. 1993 May;48(5):1082-7 [8481472.001]
  • [Cites] J Biol Chem. 1993 Aug 25;268(24):17959-66 [8349678.001]
  • [Cites] J Immunol. 1993 Nov 15;151(10):5338-47 [8228229.001]
  • [Cites] J Exp Med. 1994 Feb 1;179(2):579-88 [8294869.001]
  • [Cites] J Immunol. 1997 Sep 15;159(6):2771-81 [9300698.001]
  • (PMID = 18061684.001).
  • [ISSN] 0165-0378
  • [Journal-full-title] Journal of reproductive immunology
  • [ISO-abbreviation] J. Reprod. Immunol.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / HD039215-05; United States / NICHD NIH HHS / HD / R01 HD039215; United States / NICHD NIH HHS / HD / HD39215; United States / NICHD NIH HHS / HD / R01 HD039215-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 0 / Molecular Chaperones; 0 / Peptides; 0 / Q surface antigens; 0 / Tap1 protein, mouse; 0 / beta 2-Microglobulin
  • [Other-IDs] NLM/ NIHMS51787; NLM/ PMC2459227
  •  go-up   go-down


23. Salem PA, Estephan FF: Immunoproliferative small intestinal disease: current concepts. Cancer J; 2005 Sep-Oct;11(5):374-82
The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for immunoproliferative small intestinal disease .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoproliferative small intestinal disease: current concepts.
  • Immunoproliferative small intestinal disease is a distinctive lymphoproliferative disorder.
  • Among these disorders, it is the only disease associated with a specific and characteristic abnormal protein, and also an identifiable, at least in some patients, early phase with a benign-looking histo-pathologic expression.
  • Whether the disease at this stage is malignant or not is not known.
  • This observation is significant and raises the question of chemoprevention in lymphomas.
  • In contrast to primary nonimmunoproliferative small intestinal lymphomas, in which the pathology in the intestine is usually focal and involving specific segments of the intestine and leaving the segments between the involved areas free of disease, the pathology in immunoproliferative small intestinal disease is diffuse, with a mucosal cellular infiltrate involving large segments of the intestine and sometimes the entire length of the intestine, thus producing malabsorption.
  • Preliminary recent epidemiological data have shown a decrease in the incidence of this disease in endemic areas, and therefore environmental factors are suspected to play a major role in its pathogenesis.
  • Additional research is indicated not only to understand this specific lymphoproliferative disorder but also to understand lymphomas in general.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16259867.001).
  • [ISSN] 1528-9117
  • [Journal-full-title] Cancer journal (Sudbury, Mass.)
  • [ISO-abbreviation] Cancer J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 54
  •  go-up   go-down


24. Miron I, Mihăilă D, Aprodu G, Miron L, Plămădeală P, Moisă SM: Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy. Rom J Morphol Embryol; 2009;50(4):733-8
MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy.
  • The authors present a case of colonic monoblastic sarcoma, previously treated for other digestive abnormalities (malabsorbtion, Hirschprung's disease).
  • Important similitudes with immunoproliferative small intestinal disease (IPSID) lymphoma were demonstrated for this patient (male, 2-year-old).
  • Some particularities of this case are the young age and the extremely rapid development of the malignant disease in a patient with no previous signs of acute non-lymphoblastic leukemia.
  • The initial diagnosis was of malabsorbtion syndrome, based on the clinical exam at presentation, and then the patient was thought to have a form of Hirschprung's disease, due to a functional intestinal disorder (slow transit).
  • After the necropsy, pathologists diagnosed an immunoproliferative small intestinal disease, and four years later, they performed a more appropriate pathological exam, which explained better clinical symptoms associated to this complex case.
  • [MeSH-major] Colonic Neoplasms / diagnosis. Immunoproliferative Small Intestinal Disease / diagnosis. Sarcoma / diagnosis
  • [MeSH-minor] Child, Preschool. Diagnosis, Differential. Hirschsprung Disease / diagnosis. Humans. Malabsorption Syndromes / diagnosis. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19942975.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Romania
  •  go-up   go-down


25. Wahner-Roedler DL, Kyle RA: Heavy chain diseases. Best Pract Res Clin Haematol; 2005;18(4):729-46
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Heavy chain diseases.
  • Heavy chain diseases (HCDs) are rare B-cell lymphoplasma-cell proliferative disorders characterized by production of truncated monoclonal immunoglobulin heavy chains without associated light chains.
  • HCDs involving the three main immunoglobulin classes have been described; alpha-HCD is the most common and has the most uniform presentation, gamma- and mu-HCDs have variable clinical presentations and histopathologic features.
  • HCDs can be thought of as variant types of non-Hodgkin lymphoma: alpha-HCD presents as an extranodal marginal-zone lymphoma of mucosa-associated lymph-node tissue, gamma-HCD as lymphoplasmacytoid non-Hodgkin lymphoma, and mu-HCD as small lymphocytic non-Hodgkin lymphoma or chronic lymphocytic leukemia.
  • Diagnosis of HCD requires documentation of a deleted immunoglobulin heavy chain without a bound light chain in the serum or urine.
  • Prognosis is variable, and no standardized effective treatment programs are available except for alpha-HCD, which in its early stage may respond to antibiotics.
  • [MeSH-major] Heavy Chain Disease / diagnosis
  • [MeSH-minor] Clinical Laboratory Techniques. Humans. Immunoglobulin Heavy Chains / genetics. Lymphoproliferative Disorders / etiology. Prognosis

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16026747.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains
  • [Number-of-references] 38
  •  go-up   go-down


26. Hendriksen SW, van Leengoed LA, Roest HI, van Nes A: [Neonatal diarrhoea in pigs: alpha- and beta2-toxin produced by Clostridium perfringens]. Tijdschr Diergeneeskd; 2006 Dec 15;131(24):910-3
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Neonatal diarrhoea in pigs: alpha- and beta2-toxin produced by Clostridium perfringens].
  • [Transliterated title] Neonatale diarree bij biggen: alpha- en beta2-toxine producerende Clostridium perfringens.
  • Toxin typing by polymerase chain reaction led to the detection of genes encoding a-toxin (cpa) and beta2-toxin (cpb2).
  • Surprisingly, alpha- and beta2-toxin-producing C. perfringens was isolated from all tested herds with piglets with neonatal diarrhoea.
  • [MeSH-major] Bacterial Toxins / biosynthesis. Clostridium Infections / veterinary. Clostridium perfringens / metabolism. Diarrhea / veterinary. Swine Diseases / microbiology
  • [MeSH-minor] Animals. Animals, Newborn / microbiology. Calcium-Binding Proteins / genetics. Calcium-Binding Proteins / isolation & purification. Disease Outbreaks / veterinary. Netherlands / epidemiology. Polymerase Chain Reaction. Swine. Type C Phospholipases / genetics. Type C Phospholipases / isolation & purification. Vaccination / veterinary

  • MedlinePlus Health Information. consumer health - Diarrhea.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17278609.001).
  • [ISSN] 0040-7453
  • [Journal-full-title] Tijdschrift voor diergeneeskunde
  • [ISO-abbreviation] Tijdschr Diergeneeskd
  • [Language] dut
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / Calcium-Binding Proteins; 0 / cpb2 protein, Clostridium perfringens; EC 3.1.4.- / Type C Phospholipases; EC 3.1.4.3 / alpha toxin, Clostridium perfringens
  •  go-up   go-down


27. Du MQ: MALT lymphoma : recent advances in aetiology and molecular genetics. J Clin Exp Hematop; 2007 Nov;47(2):31-42

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MALT lymphoma : recent advances in aetiology and molecular genetics.
  • Mucosa-associated lymphoid tissue (MALT) lymphoma is a common low grade B-cell lymphoma arising from a background of chronic inflammatory disease at a number of mucosal sites.
  • Those originating in the stomach are causatively linked to Helicobacter pylori infection and eradication of the bacterium with antibiotics leads to long-term complete regression of the lymphoma in aproximately 70% of cases.
  • Now, there is further evidence of linking Campylobacter jejuni, Borrelia burgdorferi and Chlamydia psittaci infection with immunoproliferative small intestine disease, MALT lymphoma of the skin and ocular adnexa respectively. t(11;18)/API2-MALT1, t(1;14)/IGH-BCL10, t(14;18)/IGH-MALT1 and t(3;14)/IGH-FOXP1 occur at considerably variable incidences in MALT lymphomas of different sites.
  • The first three chromosome translocations are specifically associated with the MALT lymphoma entity and the oncogenic products of these translocations have been shown to target a common molecular pathway, i.e. the nuclear factor-kappaB pathway.
  • Here, I review the recent advances in our understanding of the association of microbial pathogens with MALT lymphoma of various sites and the molecular genetics underlying the lymphoma development.
  • [MeSH-major] Lymphoma, B-Cell, Marginal Zone / genetics. Lymphoma, B-Cell, Marginal Zone / microbiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18040143.001).
  • [ISSN] 1346-4280
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Number-of-references] 99
  •  go-up   go-down


28. Al-Saleem T, Al-Mondhiry H: Immunoproliferative small intestinal disease (IPSID): a model for mature B-cell neoplasms. Blood; 2005 Mar 15;105(6):2274-80
The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for immunoproliferative small intestinal disease .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoproliferative small intestinal disease (IPSID): a model for mature B-cell neoplasms.
  • Immunoproliferative small intestinal disease (IPSID) was recently added to the growing list of infectious pathogen-associated human lymphomas.
  • IPSID is a variant of the B-cell lymphoma of mucosa-associated lymphoid tissue (MALT), which involves mainly the proximal small intestine resulting in malabsorption, diarrhea, and abdominal pain.
  • Geographically, IPSID is most prevalent in the Middle East and Africa.
  • IPSID lymphomas reveal excessive plasma cell differentiation and produce truncated alpha heavy chain proteins lacking the light chains as well as the first constant domain.
  • The corresponding mRNA lacks the variable heavy chain (V(H)) and the constant heavy chain 1 (C(H)1) sequences and contains deletions as well as insertions of unknown origin.
  • Cytogenetic studies demonstrated clonal rearrangements involving predominantly the heavy and light chain genes, including t(9;14) translocation involving the PAX5 gene.
  • Early-stage IPSID responds to antibiotics (30%-70% complete remission).
  • Most untreated IPSID patients progress to lymphoplasmacytic and immunoblastic lymphoma invading the intestinal wall and mesenteric lymph nodes, and may metastasize to a distant organ.
  • IPSID lymphoma shares clinical, morphologic, and molecular features with MALT lymphoma, lymphoplasmacytic lymphoma, and plasma cell neoplasms.
  • [MeSH-major] Campylobacter Infections. Campylobacter jejuni. Immunoproliferative Small Intestinal Disease. Lymphoma, B-Cell, Marginal Zone. Plasma Cells / immunology
  • [MeSH-minor] Adolescent. Adult. Africa. B-Cell-Specific Activator Protein / genetics. B-Cell-Specific Activator Protein / immunology. Child. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 9 / genetics. Chromosomes, Human, Pair 9 / immunology. Female. Humans. Immunoglobulin Light Chains / genetics. Immunoglobulin Light Chains / immunology. Immunoglobulin Variable Region / genetics. Immunoglobulin Variable Region / immunology. Immunoglobulin alpha-Chains / genetics. Immunoglobulin alpha-Chains / immunology. Intestine, Small / immunology. Intestine, Small / pathology. Lymph Nodes / immunology. Lymph Nodes / pathology. Male. Mesentery / immunology. Mesentery / pathology. Middle East. Sequence Deletion / genetics. Sequence Deletion / immunology. Translocation, Genetic / genetics. Translocation, Genetic / immunology

  • MedlinePlus Health Information. consumer health - Campylobacter Infections.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15542584.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Immunoglobulin Light Chains; 0 / Immunoglobulin Variable Region; 0 / Immunoglobulin alpha-Chains; 0 / PAX5 protein, human
  • [Number-of-references] 78
  •  go-up   go-down


29. Mutanabbi M, Noor MK, Helal MA, Rahman MH: Coeliac disease. Mymensingh Med J; 2009 Jan;18(1 Suppl):S136-139
MedlinePlus Health Information. consumer health - Celiac Disease.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coeliac disease.
  • Coeliac disease is an autoimmune disorder of the small bowel that occurs in genetically predisposed people of all ages from middle infancy.
  • Coeliac disease is caused by a reaction to gliadin, a gluten protein found in wheat.
  • Upon exposure to gliadin, the enzyme tissue transglutaminase modifies the protein and the immune system cross reacts with the bowel tissue, causing an inflammatory reaction that leads to flattening of the lining of the small intestine, which interferes with the absorption of nutrient's.
  • He had loose mucoid stool, abdominal distension, bloating and history of loss of weight for two years.
  • Along with the routine examinations foecal fat estimation, MT, USG of whole abdomen, Barium follow through, endoscopic biopsy and tissue transglutaminage IgA autoantibody was done.
  • Histopathological report was in favour of immunoproliferative small intestinal disease.
  • Tissue transglutaminage IgA autoantibody was in higher level though done in a gluten free state.
  • Symptoms of diarrhoea, abdominal distention and bloatedness gradually decreased.
  • For patients presenting with alteration of bowel habit, abdominal distension, bloating and history of weight loss for long time, the importance of considering coeliac diseases as a differential diagnosis cannot be overemphasized.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19377424.001).
  • [ISSN] 1022-4742
  • [Journal-full-title] Mymensingh medical journal : MMJ
  • [ISO-abbreviation] Mymensingh Med J
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Bangladesh
  • [Chemical-registry-number] 0 / Immunoglobulin A; 9007-90-3 / Gliadin; EC 2.3.2.13 / Transglutaminases
  •  go-up   go-down


30. Stratigos P, Kouskos E, Kouroglou M, Chrisafis I, Fois L, Mavrogiorgis A, Axiotis E, Zamtrakis S: Emergency pancreatoduodenectomy (whipple procedure) for massive upper gastrointestinal bleeding caused by a diffuse B-cell lymphoma of the duodenum: report of a case. Surg Today; 2007;37(8):680-4
MedlinePlus Health Information. consumer health - Intestinal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Emergency pancreatoduodenectomy (whipple procedure) for massive upper gastrointestinal bleeding caused by a diffuse B-cell lymphoma of the duodenum: report of a case.
  • We herein report a rare case of a massive upper gastrointestinal (GI) bleeding, caused by high-grade diffuse B-cell lymphoma of the duodenum, secondary to immunoproliferative small intestinal disease (IPSID) and treated with an emergency partial pancreatoduodenectomy.
  • An urgent abdominal ultrasound raised the suspicion of a large, possibly bleeding, neoplasm of the duodenum, which was finally confirmed by abdominal computed tomography.
  • Histologically, the tumor was a high-grade B-cell lymphoma of the duodenum.
  • The nearby small intestinal mucosa was suggestive of IPSID.
  • A massive upper GI hemorrhage from a high-grade B-cell non-Hodgkin lymphoma of the duodenum, which develops secondary to IPSID, is a very rare clinical demonstration of this disease.
  • [MeSH-major] Duodenal Neoplasms / complications. Emergency Treatment. Gastrointestinal Hemorrhage / surgery. Lymphoma, B-Cell / complications. Pancreaticoduodenectomy / methods. Upper Gastrointestinal Tract / surgery
  • [MeSH-minor] Humans. Immunoproliferative Small Intestinal Disease

  • MedlinePlus Health Information. consumer health - Gastrointestinal Bleeding.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17643214.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


31. Funchal C, Latini A, Jacques-Silva MC, Dos Santos AQ, Buzin L, Gottfried C, Wajner M, Pessoa-Pureur R: Morphological alterations and induction of oxidative stress in glial cells caused by the branched-chain alpha-keto acids accumulating in maple syrup urine disease. Neurochem Int; 2006 Dec;49(7):640-50
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Morphological alterations and induction of oxidative stress in glial cells caused by the branched-chain alpha-keto acids accumulating in maple syrup urine disease.
  • Maple syrup urine disease (MSUD) is an inherited neurometabolic disorder biochemically characterized by the accumulation of the branched-chain alpha-keto acids (BCKA) alpha-ketoisocaproic (KIC), alpha-keto-beta-methylvaleric (KMV) and alpha-ketoisovaleric (KIV) and their respective branched-chain alpha-amino acids in body fluids and tissues.
  • Finally, we observed that the morphological features caused by BCKA on C6 cells were prevented by the use of the antioxidants GSH (1.0 mM), alpha-tocopherol (trolox; 10 microM) and Nomega-nitro-L-arginine methyl ester (L-NAME; 500 microM).
  • [MeSH-major] Brain Damage, Chronic / metabolism. Cytoskeleton / metabolism. Keto Acids / metabolism. Maple Syrup Urine Disease / metabolism. Neuroglia / metabolism. Oxidative Stress / physiology

  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16822590.001).
  • [ISSN] 0197-0186
  • [Journal-full-title] Neurochemistry international
  • [ISO-abbreviation] Neurochem. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Keto Acids; 31C4KY9ESH / Nitric Oxide; EC 1.11.1.6 / Catalase; EC 1.11.1.9 / Glutathione Peroxidase; EC 1.15.1.1 / Superoxide Dismutase; GAN16C9B8O / Glutathione
  •  go-up   go-down


32. Mak JC, Ko FW, Chu CM, Leung HC, Chan HW, Cheung AH, Ip MS, Chan-Yeung M: Polymorphisms in the IL-4, IL-4 receptor alpha chain, TNF-alpha, and lymphotoxin-alpha genes and risk of asthma in Hong Kong Chinese adults. Int Arch Allergy Immunol; 2007;144(2):114-22
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymorphisms in the IL-4, IL-4 receptor alpha chain, TNF-alpha, and lymphotoxin-alpha genes and risk of asthma in Hong Kong Chinese adults.
  • BACKGROUND: Susceptibility to the development of asthma and other atopic diseases is known to be associated with genetic components.
  • However, association studies with interleukin-4 (IL-4), IL-4 receptor alpha subunit (IL-4R alpha), tumor necrosis factor-alpha (TNF-alpha) and lymphotoxin-alpha (LT-alpha) genes were inconclusive, as both positive and negative results were obtained in several populations studied.
  • We aimed to investigate the association of the polymorphisms for IL-4 (C-589T), IL-4R alpha (Gln576Arg), TNF-alpha (G-308A) and LT-alpha (A252G) genes as candidates and asthma in adult Hong Kong Chinese population.
  • METHODS: The association study was conducted in an age- and smoking status-matched case-control design in asthma patients (n = 292) and healthy controls (n = 292) using polymerase chain reaction and restriction fragment length polymorphism.
  • After stratification by atopic status, the heterozygous AG genotype of LT-alpha (A252G) was found to increase risk of asthma in atopic population [odds ratio (OR) = 2.00, 95% CI 1.09-3.67, p = 0.024].
  • When stratified by smoking status, we found increased risk of asthma with subjects carrying the heterozygous AG and homozygous GG genotypes of LT-alpha in ever-smokers (OR = 2.73, 95% CI 1.11-6.69, p = 0.028 for heterozygotes; OR = 3.34, 95% CI 1.16-9.62, p = 0.026 for homozygotes).
  • CONCLUSION: Our results suggest that the variability of LT-alpha genotypes may have potential implications for individual susceptibility to asthma in atopic or in ever-smoking Chinese adults in Hong Kong.
  • [MeSH-major] Asthma / genetics. Genetic Predisposition to Disease. Lymphotoxin-alpha / genetics
  • [MeSH-minor] Adult. Asian Continental Ancestry Group / genetics. Female. Hong Kong / ethnology. Humans. Interleukin-4 / genetics. Interleukin-4 Receptor alpha Subunit / genetics. Male. Polymorphism, Genetic. Tumor Necrosis Factor-alpha / genetics

  • Genetic Alliance. consumer health - Asthma.
  • MedlinePlus Health Information. consumer health - Asthma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2007 S. Karger AG, Basel
  • (PMID = 17536219.001).
  • [ISSN] 1423-0097
  • [Journal-full-title] International archives of allergy and immunology
  • [ISO-abbreviation] Int. Arch. Allergy Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Interleukin-4 Receptor alpha Subunit; 0 / Lymphotoxin-alpha; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4
  •  go-up   go-down


33. Vasques Vde C, Brinco F, Wajner M: Intrahippocampal administration of the branched-chain alpha-hydroxy acids accumulating in maple syrup urine disease compromises rat performance in aversive and non-aversive behavioral tasks. J Neurol Sci; 2005 May 15;232(1-2):11-21
Hazardous Substances Data Bank. DIZOCILPINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intrahippocampal administration of the branched-chain alpha-hydroxy acids accumulating in maple syrup urine disease compromises rat performance in aversive and non-aversive behavioral tasks.
  • Maple syrup urine disease (MSUD) is an inherited metabolic disease predominantly characterized by neurological dysfunction.
  • Although a variable degree of psychomotor/delay/mental retardation is found in a considerable number of MSUD patients, the mechanisms underlying the neuropathology of this disorder are yet not defined.
  • The present study investigated the effect of acute intrahippocampal administration of the branched-chain alpha-hydroxy acids (BCHA) accumulating in MSUD on rat behavior in non-aversive (open field) and aversive (inhibitory avoidance) tasks.
  • Cannulated 60-day-old male Wistar rats received bilateral intrahippocampal injection of alpha-hydroxyisocaproic acid (HIC, 1.5 micromol), alpha-hydroxyisovaleric acid (HIV, 2.5 micromol), alpha-hydroxy-beta-methyl-n-valeric acid (HMV, 1.5 micromol), or NaCl (2.5 micromol)(controls) immediately after or 10 min before training.
  • The effect of MK-801, succinate, creatine, and the antioxidants ascorbic acid plus alpha-tocopherol on the behavioral alterations provoked by HIV in the open field task revealed that only the energetic substrates (succinate and creatine) prevented these effects, reflecting a possible compromise of brain energy production by HIV.
  • The data indicate that the alpha-hydroxy acids accumulating in MSUD impair cognition and may be implicated in the neuropathology and psychomotor delay/mental retardation observed in the affected patients.
  • [MeSH-major] Avoidance Learning / drug effects. Behavior, Animal / drug effects. Hippocampus / physiology. Hydroxy Acids / metabolism. Hydroxy Acids / pharmacology. Maple Syrup Urine Disease / metabolism

  • Hazardous Substances Data Bank. SUCCINIC ACID .
  • Hazardous Substances Data Bank. CREATINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15850577.001).
  • [ISSN] 0022-510X
  • [Journal-full-title] Journal of the neurological sciences
  • [ISO-abbreviation] J. Neurol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Excitatory Amino Acid Antagonists; 0 / Hydroxy Acids; 6LR8C1B66Q / Dizocilpine Maleate; AB6MNQ6J6L / Succinic Acid; MU72812GK0 / Creatine
  •  go-up   go-down


34. Ford AQ, Heller NM, Stephenson L, Boothby MR, Keegan AD: An atopy-associated polymorphism in the ectodomain of the IL-4R(alpha) chain (V50) regulates the persistence of STAT6 phosphorylation. J Immunol; 2009 Aug 1;183(3):1607-16
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An atopy-associated polymorphism in the ectodomain of the IL-4R(alpha) chain (V50) regulates the persistence of STAT6 phosphorylation.
  • Several commonly occurring polymorphisms in the IL-4R(alpha) have been associated with atopy in humans; the Q576R and the S503P polymorphisms reside in the cytoplasmic domain, whereas the I50 to V50 polymorphism resides in the extracellular domain of the IL-4R(alpha).
  • To determine the effect of the polymorphisms on IL-4 signaling in human cells, we stably transfected the human monocytic cell line U937 with murine IL-4R(alpha) cDNA bearing the I or V at position 50 and the P503/R576 double mutant.
  • Each form of the murine IL-4R(alpha) mediated tyrosine phosphorylation of STAT6 in response to murine IL-4 treatment similar to the induction of tyrosine phosphorylation by human IL-4 signaling through the endogenous human IL-4R(alpha).
  • Blocking IL-4 signaling during the decay phase using the JAK inhibitor AG490 or the anti-IL-4R(alpha) Ab M1 abrogated the persistence of phosphorylated STAT6 observed in the V50-IL-4R(alpha)-expressing cells.
  • These results indicate that the V50 polymorphism promotes sustained STAT6 phosphorylation and that this process is mediated by continued engagement of IL-4R(alpha), suggesting enhanced responses of V50 IL-4R when IL-4 is limiting.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Immunol. 1999 Dec 15;163(12):6876-83 [10586089.001]
  • [Cites] Cell. 2008 Jan 25;132(2):259-72 [18243101.001]
  • [Cites] Am J Hum Genet. 2000 Feb;66(2):517-26 [10677312.001]
  • [Cites] J Med Genet. 2000 May;37(5):382-4 [10905893.001]
  • [Cites] Blood. 2001 Aug 1;98(3):880-2 [11468192.001]
  • [Cites] J Immunol. 2002 Aug 1;169(3):1604-10 [12133990.001]
  • [Cites] Biochim Biophys Acta. 2002 Nov 11;1592(3):237-50 [12421669.001]
  • [Cites] J Biol Chem. 2003 Feb 7;278(6):3903-11 [12459556.001]
  • [Cites] Respir Res. 2002;3:24 [12204103.001]
  • [Cites] Science. 2003 Jun 6;300(5625):1527-8 [12791978.001]
  • [Cites] J Immunol. 2004 Jan 15;172(2):1092-8 [14707083.001]
  • [Cites] J Immunol. 2004 Oct 1;173(7):4523-8 [15383584.001]
  • [Cites] Int J Cancer. 1976 May 15;17(5):565-77 [178611.001]
  • [Cites] J Biol Chem. 1989 Apr 25;264(12):6984-9 [2523386.001]
  • [Cites] J Immunol. 1990 Jun 1;144(11):4212-7 [1692858.001]
  • [Cites] J Immunol. 1991 Jan 15;146(2):592-8 [1702807.001]
  • [Cites] Immunology. 1992 Jan;75(1):143-9 [1537590.001]
  • [Cites] Science. 1993 Dec 17;262(5141):1880-3 [8266078.001]
  • [Cites] EMBO J. 1994 Mar 15;13(6):1350-6 [8137819.001]
  • [Cites] Annu Rev Immunol. 1994;12:635-73 [7912089.001]
  • [Cites] Biochem Biophys Res Commun. 1995 Jan 17;206(2):694-702 [7826389.001]
  • [Cites] Adv Exp Med Biol. 1994;365:225-32 [7887307.001]
  • [Cites] Immunol Today. 1996 Mar;17(3):108-10 [8820266.001]
  • [Cites] J Biol Chem. 1997 Apr 11;272(15):10212-9 [9092569.001]
  • [Cites] J Exp Med. 1997 Nov 3;186(9):1419-29 [9348299.001]
  • [Cites] N Engl J Med. 1997 Dec 11;337(24):1720-5 [9392697.001]
  • [Cites] Nat Genet. 1998 Jun;19(2):119-20 [9620765.001]
  • [Cites] J Immunol. 1999 Feb 1;162(3):1227-31 [9973373.001]
  • [Cites] J Immunol. 1999 Apr 15;162(8):4385-9 [10201973.001]
  • [Cites] Immunology. 1999 Mar;96(3):365-71 [10233717.001]
  • [Cites] Annu Rev Immunol. 1999;17:701-38 [10358772.001]
  • [Cites] Am J Respir Crit Care Med. 1999 Jul;160(1):342-5 [10390422.001]
  • [Cites] Eur J Biochem. 1999 Oct 1;265(1):457-65 [10491204.001]
  • [Cites] Immunogenetics. 2005 Feb;56(11):808-17 [15712015.001]
  • [Cites] J Clin Periodontol. 2005 May;32(5):474-9 [15842262.001]
  • [Cites] Immunogenetics. 2005 Oct;57(9):644-54 [16189667.001]
  • [Cites] Int J Immunogenet. 2005 Dec;32(6):383-8 [16313303.001]
  • [Cites] Arthritis Rheum. 2006 May;54(5):1491-500 [16646030.001]
  • [Cites] J Allergy Clin Immunol. 2006 Sep;118(3):627-34 [16950281.001]
  • [Cites] Immunol Today. 2000 Feb;21(2):60-4 [10652462.001]
  • (PMID = 19592641.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI038985-13; United States / NIAID NIH HHS / AI / R01 AI038985; United States / NHLBI NIH HHS / HL / T32 HL007698; United States / NHLBI NIH HHS / HL / HL007698-13; United States / NHLBI NIH HHS / HL / T32 HL007698-12; United States / NIAID NIH HHS / AI / R01 AI038985-14; United States / NIAID NIH HHS / AI / R01 AI038985-15; United States / NHLBI NIH HHS / HL / T32 HL007698-15; United States / NHLBI NIH HHS / HL / T32 HL007698-16; United States / NIAID NIH HHS / AI / AI038985-15; United States / NIAID NIH HHS / AI / AI038985-11; United States / NHLBI NIH HHS / HL / HL007698-12; United States / NIAID NIH HHS / AI / AI038985; United States / NIAID NIH HHS / AI / R01 AI038985-11; United States / NHLBI NIH HHS / HL / T32HL007698; United States / NHLBI NIH HHS / HL / HL007698-14; United States / NIAID NIH HHS / AI / R29 AI038985; United States / NIAID NIH HHS / AI / AI038985-13; United States / NHLBI NIH HHS / HL / T32 HL007698-14; United States / NIAID NIH HHS / AI / AI038985-10; United States / NHLBI NIH HHS / HL / HL007698-16; United States / NHLBI NIH HHS / HL / HL007698-15; United States / NIAID NIH HHS / AI / R01 AI038985-12A1; United States / NIAID NIH HHS / AI / R01 AI038985-10; United States / NIAID NIH HHS / AI / AI038985-14; United States / NIAID NIH HHS / AI / AI038985-12A1; United States / NHLBI NIH HHS / HL / T32 HL007698-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Interleukin-4; 0 / STAT6 Transcription Factor; 0 / STAT6 protein, human
  • [Other-IDs] NLM/ NIHMS144498; NLM/ PMC2751580
  •  go-up   go-down


35. Evan AP, Bledsoe S, Worcester EM, Coe FL, Lingeman JE, Bergsland KJ: Renal inter-alpha-trypsin inhibitor heavy chain 3 increases in calcium oxalate stone-forming patients. Kidney Int; 2007 Dec;72(12):1503-11
Hazardous Substances Data Bank. HYALURONIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Renal inter-alpha-trypsin inhibitor heavy chain 3 increases in calcium oxalate stone-forming patients.
  • Inter-alpha-trypsin inhibitor heavy-chain proteins bind to the protease inhibitor bikunin and to hyaluronan, stabilizes extracellular matrix in various tissues, and also inhibits calcium oxalate crystallization in vitro.
  • In both normal and stone-forming patients, we found heavy chain 3 and hyaluronan in the interstitial matrix of the kidney.
  • In stone formers, heavy chain 3 was also present in collecting duct, thin loop, and interstitial cells.
  • Heavy chain 3 and osteopontin colocalized in plaque matrix and urothelial cells.
  • Within individual plaque spherules, heavy chain 3 was found in the matrix layer while osteopontin was located along the crystal-matrix interface.
  • Bikunin was present only in the collecting duct apical membranes and the loop cell cytoplasm of stone formers colocalizing with osteopontin and heavy chain 3.
  • Widespread heavy chain 3 was only present in stone formers, whereas osteopontin was similarly expressed in normal and stone-forming subjects except for its localization in plaques of the stone formers.
  • This is consistent with studies linking inter-alpha-trypsin inhibitor components to human stone disease, although their role is still unclear.
  • Heavy chain 3 may also play a role in stabilizing hyaluronan in the renal interstitial matrix.
  • [MeSH-major] Alpha-Globulins / metabolism. Calcium Oxalate / urine. Urinary Calculi / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17898697.001).
  • [ISSN] 0085-2538
  • [Journal-full-title] Kidney international
  • [ISO-abbreviation] Kidney Int.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P01 DK56788
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alpha-Globulins; 0 / alpha-1-microglobulin; 106441-73-0 / Osteopontin; 2612HC57YE / Calcium Oxalate; 39346-44-6 / inter-alpha-inhibitor; 9004-61-9 / Hyaluronic Acid
  •  go-up   go-down


36. Hernandez OM, Jones M, Guzman G, Szczesna-Cordary D: Myosin essential light chain in health and disease. Am J Physiol Heart Circ Physiol; 2007 Apr;292(4):H1643-54
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myosin essential light chain in health and disease.
  • The essential light chain of myosin (ELC) is known to be important for structural stability of the alpha-helical lever arm domain of the myosin head, but its function in striated muscle contraction is poorly understood.
  • This review summarizes the functional roles of striated muscle ELC in normal healthy muscle and in disease.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17142342.001).
  • [ISSN] 0363-6135
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL071778; United States / NHLBI NIH HHS / HL / R01 HL071778-01A1; United States / NHLBI NIH HHS / HL / HL071778-04; United States / NHLBI NIH HHS / HL / R01 HL071778-04; United States / NHLBI NIH HHS / HL / HL-071778
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myosin Light Chains
  • [Number-of-references] 113
  •  go-up   go-down


37. Emadi S, Barkhordarian H, Wang MS, Schulz P, Sierks MR: Isolation of a human single chain antibody fragment against oligomeric alpha-synuclein that inhibits aggregation and prevents alpha-synuclein-induced toxicity. J Mol Biol; 2007 May 11;368(4):1132-44
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolation of a human single chain antibody fragment against oligomeric alpha-synuclein that inhibits aggregation and prevents alpha-synuclein-induced toxicity.
  • Protein misfolding and aggregation are pathological aspects of numerous neurodegenerative diseases.
  • Aggregates of alpha-synuclein are major components of the Lewy bodies and Lewy neurites associated with Parkinson's Disease (PD).
  • A natively unfolded protein, alpha-synuclein can adopt different aggregated morphologies, including oligomers, protofibrils and fibrils.
  • The small oligomeric aggregates have been shown to be particularly toxic.
  • Antibodies that neutralize the neurotoxic aggregates without interfering with beneficial functions of monomeric alpha-synuclein can be useful therapeutics.
  • We were able to isolate single chain antibody fragments (scFvs) from a phage displayed antibody library against the target antigen morphology using a novel biopanning technique that utilizes atomic force microscopy (AFM) to image and immobilize specific morphologies of alpha-synuclein.
  • The scFv described here binds only to an oligomeric form of alpha-synuclein and inhibits both aggregation and toxicity of alpha-synuclein in vitro.
  • This scFv can have potential therapeutic value in controlling misfolding and aggregation of alpha-synuclein in vivo when expressed intracellularly in dopaminergic neurons as an intrabody.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Protein Eng Des Sel. 2006 Nov;19(11):497-502 [16984950.001]
  • [Cites] Methods Enzymol. 2006;413:326-44 [17046404.001]
  • [Cites] J Biol Chem. 2000 Nov 3;275(44):34328-34 [10915790.001]
  • [Cites] Mol Cell Neurosci. 2001 Jan;17(1):141-50 [11161475.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4764-9 [11296304.001]
  • [Cites] J Biol Chem. 2001 Jan 26;276(4):2380-6 [11060312.001]
  • [Cites] J Neurochem. 2007 Jan;100(1):23-35 [17116235.001]
  • [Cites] Science. 2000 Feb 18;287(5456):1265-9 [10678833.001]
  • [Cites] Nature. 2000 Mar 23;404(6776):394-8 [10746727.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4897-902 [10781096.001]
  • [Cites] Brain Res. 2000 Jun 2;866(1-2):33-43 [10825478.001]
  • [Cites] Neurobiol Dis. 2000 Jun;7(3):192-200 [10860784.001]
  • [Cites] Nucleic Acids Res. 2000 Sep 15;28(18):3472-7 [10982865.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 26;97(20):10701-5 [10984501.001]
  • [Cites] Methods Enzymol. 2000;326:461-79 [11036658.001]
  • [Cites] Biochemistry. 2001 Jul 3;40(26):7812-9 [11425308.001]
  • [Cites] FEBS Lett. 2001 Jul 6;500(3):105-8 [11445065.001]
  • [Cites] Neuron. 2001 Oct 25;32(2):213-23 [11683992.001]
  • [Cites] J Biol Chem. 2001 Nov 23;276(47):44284-96 [11553618.001]
  • [Cites] Biochemistry. 2002 Feb 5;41(5):1502-11 [11814343.001]
  • [Cites] Nat Cell Biol. 2002 Feb;4(2):160-4 [11813001.001]
  • [Cites] J Biol Chem. 2002 May 3;277(18):16116-23 [11850416.001]
  • [Cites] Nat Med. 2002 Jun;8(6):600-6 [12042811.001]
  • [Cites] Nature. 2002 Jul 18;418(6895):291 [12124613.001]
  • [Cites] J Biol Chem. 2002 Aug 9;277(32):28512-20 [12032141.001]
  • [Cites] Biochemistry. 2002 Aug 13;41(32):10209-17 [12162735.001]
  • [Cites] Biochemistry. 2002 Nov 19;41(46):13782-90 [12427041.001]
  • [Cites] J Biol Chem. 2002 Dec 13;277(50):48984-92 [12351643.001]
  • [Cites] Biochemistry. 2003 Apr 8;42(13):3696-700 [12667059.001]
  • [Cites] Science. 2003 Apr 18;300(5618):486-9 [12702875.001]
  • [Cites] J Mol Biol. 2003 Jun 13;329(4):763-78 [12787676.001]
  • [Cites] Biochemistry. 2003 Jul 8;42(26):7871-8 [12834338.001]
  • [Cites] Mol Ther. 2003 Sep;8(3):355-66 [12946308.001]
  • [Cites] Science. 2003 Oct 31;302(5646):841 [14593171.001]
  • [Cites] Neuron. 2003 Oct 30;40(3):453-6 [14642269.001]
  • [Cites] Ann Neurol. 2004 Feb;55(2):164-73 [14755719.001]
  • [Cites] Brain Res Mol Brain Res. 2004 Feb 5;121(1-2):141-5 [14969746.001]
  • [Cites] Biochemistry. 2004 Mar 16;43(10):2871-8 [15005622.001]
  • [Cites] J Biol Chem. 2004 Jun 11;279(24):25497-502 [15044495.001]
  • [Cites] FASEB J. 2004 Aug;18(11):1315-7 [15180968.001]
  • [Cites] Nucleic Acids Res. 1985 Jun 25;13(12):4431-43 [2989795.001]
  • [Cites] Anal Biochem. 1987 Nov 1;166(2):368-79 [2449095.001]
  • [Cites] J Mol Biol. 1992 Sep 20;227(2):381-8 [1404359.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Aug 15;90(16):7889-93 [8356098.001]
  • [Cites] Neuron. 1995 Feb;14(2):467-75 [7857654.001]
  • [Cites] J Neurochem. 1995 Jul;65(1):218-27 [7790863.001]
  • [Cites] Science. 1997 Jun 27;276(5321):2045-7 [9197268.001]
  • [Cites] Nature. 1997 Aug 28;388(6645):839-40 [9278044.001]
  • [Cites] Baillieres Clin Neurol. 1997 Apr;6(1):15-36 [9426866.001]
  • [Cites] Neurology. 1998 Feb;50(2):318 and 16 pages following [9484345.001]
  • [Cites] Am J Pathol. 1998 Apr;152(4):879-84 [9546347.001]
  • [Cites] J Biol Chem. 1998 Apr 17;273(16):9443-9 [9545270.001]
  • [Cites] Ann Neurol. 1998 Sep;44(3):415-22 [9749615.001]
  • [Cites] FEBS Lett. 1998 Oct 9;436(3):309-12 [9801138.001]
  • [Cites] Nat Med. 1998 Nov;4(11):1318-20 [9809558.001]
  • [Cites] Acta Neuropathol. 1998 Nov;96(5):445-52 [9829807.001]
  • [Cites] J Biol Chem. 1999 Mar 19;274(12):7619-22 [10075647.001]
  • [Cites] J Biol Chem. 1999 Apr 2;274(14):9843-6 [10092675.001]
  • [Cites] N Engl J Med. 1999 Jun 24;340(25):1970-80 [10379022.001]
  • [Cites] Brain Pathol. 1999 Oct;9(4):721-32 [10517510.001]
  • [Cites] Neurology. 1999 Oct 12;53(6):1284-91 [10522886.001]
  • [Cites] Mol Ther. 2004 Dec;10(6):1023-31 [15564134.001]
  • [Cites] Neuron. 2005 Jun 16;46(6):857-68 [15953415.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 9;102(32):11563-8 [16061794.001]
  • [Cites] FASEB J. 2006 Mar;20(3):419-25 [16507759.001]
  • [Cites] Biotechnol Prog. 2006 May-Jun;22(3):919-22 [16739981.001]
  • (PMID = 17391701.001).
  • [ISSN] 0022-2836
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01 AG017984; United States / NIA NIH HHS / AG / R01 AG017984-01; United States / NIA NIH HHS / AG / R01 AG017984-02; United States / NIA NIH HHS / AG / R01 AG017984-04; United States / NIA NIH HHS / AG / R01 AG017984-03; United States / NIA NIH HHS / AG / AG17984
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Variable Region; 0 / Peptide Library; 0 / alpha-Synuclein
  • [Other-IDs] NLM/ NIHMS22525; NLM/ PMC2235820
  •  go-up   go-down


38. Soriano A, Lozano F, Oliva H, García F, Nomdedéu M, De Lazzari E, Rodríguez C, Barrasa A, Lorenzo JI, Del Romero J, Plana M, Miró JM, Gatell JM, Vives J, Gallart T: Polymorphisms in the interleukin-4 receptor alpha chain gene influence susceptibility to HIV-1 infection and its progression to AIDS. Immunogenetics; 2005 Oct;57(9):644-54
SciCrunch. OMIM: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymorphisms in the interleukin-4 receptor alpha chain gene influence susceptibility to HIV-1 infection and its progression to AIDS.
  • Our objective is to investigate whether single-nucleotide polymorphisms (SNPs) in the IL-4 receptor alpha chain gene (IL4RA) affect HIV infection and its progression to AIDS.
  • The I50V SNP in exon 5 and the haplotypes of six SNPs in exon 12 (E375A, C406R, S411L, S478P, Q551R, and V554I) were studied by polymerase chain reaction and sequencing in 30 HIV+ long-term nonprogressors (LTNP), 36 HIV+ typical progressors (TP), 55 highly exposed but uninfected individuals (EU), 25 EU-sexuals (EU-Sex; mostly women) and 30 EU-hemophiliacs (EU-Hem; hepatitis C virus+), and 97 healthy controls (HC), all Caucasians and lacking CCR5Delta32 homozygosity.
  • [MeSH-major] Genetic Predisposition to Disease. HIV Infections / genetics. Polymorphism, Single Nucleotide. Receptors, Cell Surface / genetics
  • [MeSH-minor] Acquired Immunodeficiency Syndrome / genetics. Exons. Female. Gene Frequency. Genotype. Haplotypes. Homozygote. Humans. Interleukin-4 Receptor alpha Subunit. Male. Protein Subunits / genetics


39. Semenova EV, Shadrina MI, Slominskiĭ PA, Illarioshkin SN, Bagyeva GKh, Karabanov AV, Ivanova-Smolenskaia IA, Limborskaia SA: [Analysis of the alpha-synuclein gene dosage variation associated with autosomal dominant form of ParkinsonTs disease]. Genetika; 2009 Apr;45(4):573-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Analysis of the alpha-synuclein gene dosage variation associated with autosomal dominant form of ParkinsonTs disease].
  • Fifty-two patients that had ParkinsonTs disease with autosomal dominant type of inheritance were analyzed for the presence of duplications and triplications in exons 4--6 of alpha-synuclein gene using real-time PCR with Taq-Man probes.
  • No mutations involving the examined exons dosage were revealed in alpha-synuclein gene.
  • Thus, mutations modifying copy number of alpha-synuclein gene do not significantly affect the pathogenesis of the autosomal dominant form of ParkinsonTs disease in patients from Russia.
  • [MeSH-major] Exons / genetics. Gene Dosage. Parkinsonian Disorders / genetics. alpha-Synuclein / genetics
  • [MeSH-minor] Female. Humans. Male. Reverse Transcriptase Polymerase Chain Reaction / methods. Russia

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19507712.001).
  • [ISSN] 0016-6758
  • [Journal-full-title] Genetika
  • [ISO-abbreviation] Genetika
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / alpha-Synuclein
  •  go-up   go-down


40. Nava MP, Trejo JM, Aguilar-Luna C, Barros-Núñez P, Chávez Mde L, Magaña MT, Perea J, Ibarra B: Molecular characterization of the--SEA alpha thalassemia allele in Mexican patients with HbH disease. Rev Invest Clin; 2006 Jul-Aug;58(4):313-7
Genetic Alliance. consumer health - Thalassemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular characterization of the--SEA alpha thalassemia allele in Mexican patients with HbH disease.
  • Alpha-Thalassemia is one of the most prevalent hemoglobin disorders in the world, in South-East Asians, the --SEA allele is widely found in the HbH disease patients.
  • The purpose of this work is to describe the molecular characteristics of Hemoglobin H disease in three patients from two Mexican families, as well to analyze the DNA sequence of the --SEA allele to determine the precise site of the crossover.
  • The -alpha 3.7 and --SEA alleles were identified using an established long-PCR method modified in our laboratory.
  • DNA analysis through the breakpoint sites of the SEA allele in both families showed the 5' breakpoint at the third base of codon 28 in the psi alpha 2 gene and the 3' breakpoint within an Alu-Jo sequence, 1,328 nucleotides upstream of the 3'HVR.
  • [MeSH-major] Hemoglobin H / genetics. alpha-Thalassemia / genetics
  • [MeSH-minor] Alleles. Child. DNA Mutational Analysis. Female. Humans. Male. Mexico. Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Alpha-Thalassemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17146943.001).
  • [ISSN] 0034-8376
  • [Journal-full-title] Revista de investigación clínica; organo del Hospital de Enfermedades de la Nutrición
  • [ISO-abbreviation] Rev. Invest. Clin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Mexico
  • [Chemical-registry-number] 9034-79-1 / Hemoglobin H
  •  go-up   go-down


41. SanGiovanni JP, Chew EY: The role of omega-3 long-chain polyunsaturated fatty acids in health and disease of the retina. Prog Retin Eye Res; 2005 Jan;24(1):87-138
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of omega-3 long-chain polyunsaturated fatty acids in health and disease of the retina.
  • In this work we advance the hypothesis that omega-3 (omega-3) long-chain polyunsaturated fatty acids (LCPUFAs) exhibit cytoprotective and cytotherapeutic actions contributing to a number of anti-angiogenic and neuroprotective mechanisms within the retina. omega-3 LCPUFAs may modulate metabolic processes and attenuate effects of environmental exposures that activate molecules implicated in pathogenesis of vasoproliferative and neurodegenerative retinal diseases.
  • We discuss the relationship of LCPUFAs with these bioactivators and bioactive compounds in the context of three blinding retinal diseases of public health significance that exhibit both vascular and neural pathology.
  • What evidence exists to suggest that LCPUFAs modulate factors and processes implicated in diseases of the vascular and neural retina?
  • DHA activates a number of nuclear hormone receptors that operate as transcription factors for molecules that modulate reduction-oxidation-sensitive and proinflammatory genes; these include the peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and the retinoid X receptor.
  • In the case of PPAR-alpha, this action is thought to prevent endothelial cell dysfunction and vascular remodeling through inhibition of: vascular smooth muscle cell proliferation, inducible nitric oxide synthase production, interleukin-1 induced cyclooxygenase (COX)-2 production, and thrombin-induced endothelin 1 production.
  • [MeSH-major] Fatty Acids, Omega-3 / physiology. Retina / metabolism. Retinal Diseases / metabolism

  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15555528.001).
  • [ISSN] 1350-9462
  • [Journal-full-title] Progress in retinal and eye research
  • [ISO-abbreviation] Prog Retin Eye Res
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 EY999999
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Fatty Acids, Omega-3
  • [Number-of-references] 454
  •  go-up   go-down


42. Sugawara K, Ohno K, Saito S, Sakuraba H: Structural characterization of mutant alpha-galactosidases causing Fabry disease. J Hum Genet; 2008;53(9):812-24
Nature Publishing Group. Nature Publishing Group (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structural characterization of mutant alpha-galactosidases causing Fabry disease.
  • Fabry disease is an inborn error of glycolipid catabolism resulting from lesions in the gene encoding alpha-galactosidase (GLA).
  • To elucidate the basis of Fabry disease, we constructed structural models of mutant GLAs responsible for the disease and calculated indexes, i.e., the numbers of atoms affected in the main chain and side chain of each mutant GLA, the root-mean-square distance values, and the solvent-accessible surface-area values, based on 212 Fabry amino acid substitutions previously reported (196 classic and 16 variant).
  • As two therapeutic options, enzyme replacement and enzyme enhancement, are now available for this disease, proper prediction of the natural outcome and therapeutic efficiency based on the molecular evidence for individual cases are critical for patients' quality of life.
  • On the other hand, structural changes in the variant Fabry group were small or localized on the surface of the molecule far away from the active site.
  • We focused on structural changes due to amino acid substitutions for which substrate analogues are effective for improving the stability or transportation of mutant GLAs, and the results of the study revealed that they are small or localized on the molecular surface, regardless of the phenotype.
  • Coloring of affected atoms based on distances between wild type and mutant ones clearly showed the characteristic structural changes in the GLA protein geographically and subquantitatively.
  • Structural investigation is useful for elucidation of the basis of Fabry disease and predicting disease outcome.
  • [MeSH-major] Fabry Disease / genetics. alpha-Galactosidase / chemistry. alpha-Galactosidase / genetics

  • Genetic Alliance. consumer health - BabyFirstTest - Fabry Disease.
  • Genetic Alliance. consumer health - Fabry Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18633574.001).
  • [ISSN] 1434-5161
  • [Journal-full-title] Journal of human genetics
  • [ISO-abbreviation] J. Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Mutant Proteins; EC 3.2.1.22 / alpha-Galactosidase
  •  go-up   go-down


43. Terwijn M, Feller N, van Rhenen A, Kelder A, Westra G, Zweegman S, Ossenkoppele G, Schuurhuis GJ: Interleukin-2 receptor alpha-chain (CD25) expression on leukaemic blasts is predictive for outcome and level of residual disease in AML. Eur J Cancer; 2009 Jun;45(9):1692-9
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-2 receptor alpha-chain (CD25) expression on leukaemic blasts is predictive for outcome and level of residual disease in AML.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Interleukin-2 Receptor alpha Subunit / metabolism. Leukemia, Myeloid, Acute / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19321337.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Interleukin-2 Receptor alpha Subunit
  •  go-up   go-down


44. Malfait F, Symoens S, De Backer J, Hermanns-Lê T, Sakalihasan N, Lapière CM, Coucke P, De Paepe A: Three arginine to cysteine substitutions in the pro-alpha (I)-collagen chain cause Ehlers-Danlos syndrome with a propensity to arterial rupture in early adulthood. Hum Mutat; 2007 Apr;28(4):387-95
SciCrunch. Clinical Genomic Database: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Three arginine to cysteine substitutions in the pro-alpha (I)-collagen chain cause Ehlers-Danlos syndrome with a propensity to arterial rupture in early adulthood.
  • Mutations in the COL1A1 and COL1A2 genes, encoding the proalpha1 and 2 chains of type I collagen, cause osteogenesis imperfecta (OI) or Ehlers-Danlos syndrome (EDS) arthrochalasis type.
  • Although the majority of missense mutations in the collagen type I triple helix affect glycine residues in the Gly-Xaa-Yaa repeat, few nonglycine substitutions have been reported.
  • Two arginine-to-cysteine substitutions in the alpha1(I)-collagen chain are associated with classic EDS [R134C (p.R312C)] or autosomal dominant Caffey disease with mild EDS features [R836C (p.R1014C)].
  • Dermal fibroblasts from the patients produced disulfide-bonded alpha1(I)-dimers in approximately 20% of type I collagen, which were efficiently secreted into the medium in case of the R396C and R915C substitution.
  • Theoretical stability calculations of the collagen type I heterotrimer and thermal denaturation curves of monomeric mutant alpha1(I)-collagen chains showed minor destabilization of the collagen helix.
  • Our findings demonstrate that R-to-C substitutions in the alpha1(I) chain may result in a phenotype with propensity to arterial rupture in early adulthood.
  • This broadens the phenotypic range of nonglycine substitutions in collagen type I and has important implications for genetic counseling and follow-up of patients carrying this type of mutation.
  • [MeSH-major] Collagen Type I / genetics. Ehlers-Danlos Syndrome / complications. Ehlers-Danlos Syndrome / genetics. Rupture, Spontaneous / genetics
  • [MeSH-minor] Adolescent. Adult. Amino Acid Substitution. Arginine / genetics. Arginine / metabolism. Base Sequence. Bone Diseases, Metabolic / complications. Bone Diseases, Metabolic / genetics. Bone Diseases, Metabolic / metabolism. Collagen / genetics. Collagen Type III / genetics. Cysteine / genetics. Cysteine / metabolism. Female. Femoral Artery. Humans. Iliac Artery. Male. Molecular Sequence Data. Mutation, Missense. Protein Structure, Secondary. RNA, Messenger / genetics

  • Genetic Alliance. consumer health - Ehlers-Danlos syndrome.
  • MedlinePlus Health Information. consumer health - Ehlers-Danlos Syndrome.
  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. CYSTEINE .
  • Hazardous Substances Data Bank. (L)-ARGININE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2007 Wiley-Liss, Inc.
  • (PMID = 17211858.001).
  • [ISSN] 1098-1004
  • [Journal-full-title] Human mutation
  • [ISO-abbreviation] Hum. Mutat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / COL3A1 protein, human; 0 / Collagen Type I; 0 / Collagen Type III; 0 / RNA, Messenger; 0 / alpha 2(I) collagen; 0 / collagen type I, alpha 1 chain; 9007-34-5 / Collagen; 94ZLA3W45F / Arginine; K848JZ4886 / Cysteine
  •  go-up   go-down


45. Poutanen T, Tikanoja T, Jääskeläinen P, Jokinen E, Silvast A, Laakso M, Kuusisto J: Diastolic dysfunction without left ventricular hypertrophy is an early finding in children with hypertrophic cardiomyopathy-causing mutations in the beta-myosin heavy chain, alpha-tropomyosin, and myosin-binding protein C genes. Am Heart J; 2006 Mar;151(3):725.e1-725.e9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diastolic dysfunction without left ventricular hypertrophy is an early finding in children with hypertrophic cardiomyopathy-causing mutations in the beta-myosin heavy chain, alpha-tropomyosin, and myosin-binding protein C genes.
  • METHODS: All children (aged 1.5-16.7 years) from 14 HCM families with identified disease-causing mutations (the Arg719Trp mutation in the beta-myosin heavy chain gene [MYH7], the Asp175Asn mutation in the alpha-tropomyosin gene [TPM1], the Gln1061X mutation in the myosin-binding protein C gene [MYBPC3], and the IVS5-2A-->C mutation in the MYBPC3 gene) and 53 matched control children were examined with electrocardiography and 2- and 3-dimensional echocardiography (2DE and 3DE).
  • RESULTS: Of 53 children from HCM families, 27 (51%) had a disease-causing mutation (G+).
  • CONCLUSIONS: In children with HCM-causing mutations, signs of diastolic dysfunction are found in about half of the cases, as LVH is present only in small percentage of these children.

  • Genetic Alliance. consumer health - Cardiomyopathy.
  • Genetic Alliance. consumer health - Hypertrophic Cardiomyopathy.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16504640.001).
  • [ISSN] 1097-6744
  • [Journal-full-title] American heart journal
  • [ISO-abbreviation] Am. Heart J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / TPM1 protein, human; 0 / Tropomyosin; 0 / myosin-binding protein C; 85637-73-6 / Atrial Natriuretic Factor; EC 3.6.1.- / Ventricular Myosins
  •  go-up   go-down


46. Funchal C, Dos Santos AQ, Jacques-Silva MC, Zamoner A, Gottfried C, Wajner M, Pessoa-Pureur R: Branched-chain alpha-keto acids accumulating in maple syrup urine disease induce reorganization of phosphorylated GFAP in C6-glioma cells. Metab Brain Dis; 2005 Sep;20(3):205-17

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Branched-chain alpha-keto acids accumulating in maple syrup urine disease induce reorganization of phosphorylated GFAP in C6-glioma cells.
  • In this study we investigate the effects of the branched-chain keto acids (BCKA) alpha-ketoisocaproic (KIC), alpha-ketoisovaleric (KIV), and alpha-keto-beta-methylvaleric (KMV) acids, metabolites accumulating in maple syrup urine disease (MSUD), on the in vitro phosphorylation of glial fibrillary acidic protein (GFAP) and cytoskeletal reorganization in C6-glioma cells.
  • [MeSH-major] Cytoskeleton / metabolism. Glial Fibrillary Acidic Protein / metabolism. Glioma / metabolism. Keto Acids / metabolism. Maple Syrup Urine Disease / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16167198.001).
  • [ISSN] 0885-7490
  • [Journal-full-title] Metabolic brain disease
  • [ISO-abbreviation] Metab Brain Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Keto Acids; 1460-34-0 / alpha-keto-beta-methylvaleric acid; 759-05-7 / alpha-ketoisovalerate; 816-66-0 / alpha-ketoisocaproic acid
  •  go-up   go-down


47. Gawlik KI, Durbeej M: Transgenic overexpression of laminin alpha1 chain in laminin alpha2 chain-deficient mice rescues the disease throughout the lifespan. Muscle Nerve; 2010 Jul;42(1):30-7
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transgenic overexpression of laminin alpha1 chain in laminin alpha2 chain-deficient mice rescues the disease throughout the lifespan.
  • Several approaches to treat laminin alpha2 chain-deficient congenital muscular dystrophy (MDC1A) in mouse models have been undertaken.
  • Herein we analyze the lifespan of laminin alpha2 chain-deficient mice with transgenic overexpression of laminin alpha1 chain.
  • We show that laminin alpha2-chain-deficient animals that overexpress laminin alpha1 chain survive to up to 1.5-2 years of age.

  • MedlinePlus Health Information. consumer health - Seniors' Health.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20544910.001).
  • [ISSN] 1097-4598
  • [Journal-full-title] Muscle & nerve
  • [ISO-abbreviation] Muscle Nerve
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Laminin; 0 / laminin alpha 2; 151186-83-3 / laminin A; EC 2.7.3.2 / Creatine Kinase
  •  go-up   go-down


48. Funchal C, Tramontina F, Quincozes dos Santos A, Fraga de Souza D, Gonçalves CA, Pessoa-Pureur R, Wajner M: Effect of the branched-chain alpha-keto acids accumulating in maple syrup urine disease on S100B release from glial cells. J Neurol Sci; 2007 Sep 15;260(1-2):87-94
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of the branched-chain alpha-keto acids accumulating in maple syrup urine disease on S100B release from glial cells.
  • Accumulation of the branched-chain alpha-keto acids (BCKA), alpha-ketoisocaproic acid (KIC), alpha-keto-beta-methylvaleric acid (KMV) and alpha-ketoisovaleric acid (KIV) and their respective branched-chain alpha-amino acids (BCAA) occurs in tissues and biological fluids of patients affected by the neurometabolic disorder maple syrup urine disease (MSUD).
  • [MeSH-major] Brain / metabolism. Keto Acids / metabolism. Maple Syrup Urine Disease / complications. Maple Syrup Urine Disease / metabolism. Nerve Degeneration / etiology. Nerve Degeneration / metabolism. Nerve Growth Factors / metabolism. Neuroglia / metabolism. S100 Proteins / metabolism
  • [MeSH-minor] Animals. Cell Death / drug effects. Cell Death / physiology. Cell Line, Tumor. Creatine / metabolism. Creatine / pharmacology. Dose-Response Relationship, Drug. Energy Metabolism / drug effects. Energy Metabolism / physiology. Enzyme Inhibitors / pharmacology. Nitric Oxide / metabolism. Nitric Oxide Synthase Type I / antagonists & inhibitors. Nitric Oxide Synthase Type I / metabolism. Oxidation-Reduction / drug effects. Oxidative Stress / drug effects. Oxidative Stress / physiology. Protein Kinases / drug effects. Protein Kinases / metabolism. Rats. S100 Calcium Binding Protein beta Subunit

  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • Hazardous Substances Data Bank. CREATINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17499767.001).
  • [ISSN] 0022-510X
  • [Journal-full-title] Journal of the neurological sciences
  • [ISO-abbreviation] J. Neurol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Keto Acids; 0 / Nerve Growth Factors; 0 / S100 Calcium Binding Protein beta Subunit; 0 / S100 Proteins; 0 / S100b protein, rat; 31C4KY9ESH / Nitric Oxide; EC 1.14.13.39 / Nitric Oxide Synthase Type I; EC 2.7.- / Protein Kinases; MU72812GK0 / Creatine
  •  go-up   go-down


49. Hwang HY, Kim TG, Kim TY: Analysis of T cell receptor alpha-chain variable region (Valpha) usage and CDR3alpha of T cells infiltrated into lesions of psoriasis patients. Mol Immunol; 2006 Feb;43(5):420-5
MedlinePlus Health Information. consumer health - Psoriasis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of T cell receptor alpha-chain variable region (Valpha) usage and CDR3alpha of T cells infiltrated into lesions of psoriasis patients.
  • Psoriasis is a common inflammatory skin disease and is considered as T cell-mediated immune response.
  • In this study, we analyzed T cell receptor alpha-chain variable region (TCR Valpha) usage in the lesions of psoriasis patients using 5'-RACE.
  • Then, to identify CDR3alpha of T cells infiltrated in psoriatic lesions, we examined which type of J gene segment was rearranged with Valpha1 or Valpha7, which the expressions was specifically increased in psoriatic lesions.
  • [MeSH-major] Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor. Psoriasis / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics. T-Cell Antigen Receptor Specificity. T-Lymphocyte Subsets / immunology
  • [MeSH-minor] Amino Acid Sequence. Genetic Predisposition to Disease. HLA-C Antigens / analysis. Humans. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction. Skin / immunology. Skin / pathology

  • Genetic Alliance. consumer health - Psoriasis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16337484.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-C Antigens; 0 / HLA-C*06:02 antigen; 0 / Receptors, Antigen, T-Cell, alpha-beta
  •  go-up   go-down


50. Ateş A, Kinikli G, Düzgün N, Duman M: Lack of association of tumor necrosis factor-alpha gene polymorphisms with disease susceptibility and severity in Behçet's disease. Rheumatol Int; 2006 Feb;26(4):348-53
MedlinePlus Health Information. consumer health - Behcet's Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of association of tumor necrosis factor-alpha gene polymorphisms with disease susceptibility and severity in Behçet's disease.
  • Although it has been reported that the MHC class I molecule, HLA-B51, is a risk factor for Behçet's disease (BD), contribution of the tumor necrosis factor (TNF) genes, which are located in the vicinity of the HLA-B locus, to the genetic susceptibility for BD has yet to be elucidated.
  • The purpose of this study was to analyze the effect of TNF-alpha promoter polymorphisms at positions -308, -238 and -376 on the susceptibility, severity and clinical features of BD.
  • The TNF-alpha gene sequences from 107 patients with BD and 102 healthy subjects were amplified by the polymerase chain reaction.
  • Sequence analysis of the TNF-alpha gene locus, which contains promoter polymorphisms at positions -376, -308, and -238, was performed with a DNA sequencing kit on automated sequencer.
  • The patients were classified according to disease severity and clinical features.
  • Serum TNF-alpha level in the study groups was measured by sandwich enzyme immunoassay.
  • In patients with BD the frequencies of TNF-alpha -308 (19.4% vs 18.4%), -238 (3.7% vs 5.9%), and -376 (0.9% vs 2.9%) gene polymorphisms were not found to be significantly different from those in healthy subjects.
  • The TNF-alpha gene polymorphisms did not show any association with disease severity or clinical features.
  • Serum TNF-alpha level was significantly higher in patients with BD than in healthy controls (3.10 +/- 1.45 pg/ml vs 2.43 +/- 1.94 pg/ml, P < 0.01).
  • Serum TNF-alpha level was not found to be significantly associated with disease severity, activity, clinical findings and TNF-alpha genotypes.
  • The results of this study suggest that the TNF-alpha gene polymorphisms are unlikely to play an important role in the pathogenesis and severity of BD.
  • [MeSH-major] Behcet Syndrome / genetics. Behcet Syndrome / pathology. Polymorphism, Genetic. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adult. Female. Gene Frequency. Genetic Predisposition to Disease. Humans. Male. Polymerase Chain Reaction. Sequence Analysis, DNA. Severity of Illness Index

  • Genetic Alliance. consumer health - Behcet's Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15875188.001).
  • [ISSN] 0172-8172
  • [Journal-full-title] Rheumatology international
  • [ISO-abbreviation] Rheumatol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


51. Mahdavi MR, Kowsarian M, Karami H, Mohseni A, Vahidshahi K, Roshan P, Hojjati MT, Ebrahimzadeh MA: Prevalence of hemoglobin alpha-chain gene deletion in neonates in North of Iran. Eur Rev Med Pharmacol Sci; 2010 Oct;14(10):871-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence of hemoglobin alpha-chain gene deletion in neonates in North of Iran.
  • OBJECTIVES: Alpha-thalassemia (alpha-thal) is one of the most common genetic disorders and in some populations has prevalence as high as 30%.
  • Disorders in hemoglobin (Hb) synthesis lead to mild to severe reduction in alpha-chain synthesis.
  • Diagnosis of alpha-thal by examining fresh blood taken from umbilical cord is a simple and appropriate approach, while in later stages its diagnosis will be difficult and costly.
  • MATERIAL AND METHODS: This study examined the prevalence of alpha-thal gene deletion in neonates in Sari, Iran.
  • Prevalence of alpha-thal was calculated and statistically analyzed (p < 5%).
  • If the ratio of mean corpuscular volume (MCV) to red blood cell (RBC) count is smaller than 23, risk of alpha-thal is 2.8 fold greater than cases with an MCV/RBC ratio below 23 (p < 0.05).
  • None of the cases were reported to be positive for Hb H disease and hydrops fetalis.
  • CONCLUSIONS: Considering high prevalence of alpha-thal gene deletions in neonates in Sari hospitals, it is recommended to screen newborns for alpha-thal in this city and similar areas with such a high prevalence.
  • [MeSH-major] Gene Deletion. alpha-Globins / genetics. alpha-Thalassemia / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21222374.001).
  • [ISSN] 1128-3602
  • [Journal-full-title] European review for medical and pharmacological sciences
  • [ISO-abbreviation] Eur Rev Med Pharmacol Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Hemoglobins, Abnormal; 0 / alpha-Globins; 9056-09-1 / hemoglobin Bart's
  •  go-up   go-down


52. Navarro D, Zwingmann C, Butterworth RF: Impaired oxidation of branched-chain amino acids in the medial thalamus of thiamine-deficient rats. Metab Brain Dis; 2008 Dec;23(4):445-55
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impaired oxidation of branched-chain amino acids in the medial thalamus of thiamine-deficient rats.
  • Thiamine, in its diphosphate form, is a required cofactor for enzymes of glucose metabolism and branched-chain alpha-ketoacid dehydrogenase (BCKDH).
  • A significant regional variation in BCKDH within the TD rat brain was noted, with a higher capacity for branched-chain amino acid oxidation in FC compared to MT: BCKDH activity was significantly reduced in MT of TD rats, resulting in selective accumulation of BCAAs in this brain region.
  • Impaired branched-chain ketoacid metabolism in rats may contribute to the neuronal dysfunction and ultimate thalamic neuronal cell death observed in thiamine deficiency.
  • [MeSH-major] 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide) / metabolism. Amino Acids, Branched-Chain / metabolism. Thalamus / metabolism. Thiamine Deficiency / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18773288.001).
  • [ISSN] 0885-7490
  • [Journal-full-title] Metabolic brain disease
  • [ISO-abbreviation] Metab Brain Dis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids, Branched-Chain; 0 / Coenzymes; EC 1.2.4.4 / 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)
  •  go-up   go-down


53. Asada H, Yamagata Y, Taketani T, Matsuoka A, Tamura H, Hattori N, Ohgane J, Hattori N, Shiota K, Sugino N: Potential link between estrogen receptor-alpha gene hypomethylation and uterine fibroid formation. Mol Hum Reprod; 2008 Sep;14(9):539-45
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potential link between estrogen receptor-alpha gene hypomethylation and uterine fibroid formation.
  • Estrogen receptor-alpha (ER-alpha) is more highly expressed in uterine leiomyomas than in normal myometrium, suggesting a link between uterine leiomyomas and ER-alpha expression.
  • DNA methylation is an epigenetic mechanism of gene regulation and plays important roles in normal embryonic development and in disease progression including cancers.
  • Here, we investigated the DNA methylation status of the ER-alpha promoter region (-1188 to +229 bp) in myometrium and leiomyoma.
  • By sodium bisulfite sequencing, 49 CpG sites in the proximal promoter region of ER-alpha gene were shown to be unmethylated in both leiomyoma and normal myometrium.
  • At seven CpG sites in the distal promoter region of the ER-alpha gene, there was a variation in DNA methylation status in myometrium and leiomyoma.
  • Further analysis of the DNA methylation status by bisulfite restriction mapping among 11 paired samples of myometrium and leiomyoma indicated that CpG sites in the distal region of ER-alpha promoter are hypomethylated in leiomyomas of nine patients.
  • In those patients, ER-alpha mRNA levels tended to be higher in the leiomyoma than in the myometrium.
  • In conclusion, there was an aberrant DNA methylation status in the promoter region of ER-alpha gene in uterine leiomyoma, which may be associated with high ER-alpha mRNA expression.
  • [MeSH-major] DNA Methylation. Estrogen Receptor alpha / genetics. Leiomyoma / pathology
  • [MeSH-minor] Adult. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Cells, Cultured. CpG Islands / genetics. Enzyme Inhibitors / pharmacology. Female. Gene Expression / drug effects. Humans. Immunohistochemistry. Middle Aged. Myocytes, Smooth Muscle / cytology. Myocytes, Smooth Muscle / drug effects. Myocytes, Smooth Muscle / metabolism. Promoter Regions, Genetic / genetics. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Uterine Fibroid.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18701604.001).
  • [ISSN] 1460-2407
  • [Journal-full-title] Molecular human reproduction
  • [ISO-abbreviation] Mol. Hum. Reprod.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Estrogen Receptor alpha; M801H13NRU / Azacitidine
  •  go-up   go-down


54. Yao XS, Diao Y, Sun WB, Luo JM, Qin M, Tang XY: Analysis of the CDR3 length repertoire and the diversity of TCR alpha chain in human peripheral blood T lymphocytes. Cell Mol Immunol; 2007 Jun;4(3):215-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of the CDR3 length repertoire and the diversity of TCR alpha chain in human peripheral blood T lymphocytes.
  • Analysis of complementarity determining region 3 (CDR3) length of T lymphocyte receptors (TCRs) by immunoscope spectratyping technique has been used successfully to investigate the diversity of TCR in autoimmune diseases and infection diseases.
  • These results may be helpful to further study the recombination mechanism of human TCR genes, the TCR CDR3 gene repertoire, and the repertoire drift in health people and disease state.
  • [MeSH-major] Complementarity Determining Regions / chemistry. Complementarity Determining Regions / genetics. Genetic Variation. Receptors, Antigen, T-Cell, alpha-beta / chemistry. Receptors, Antigen, T-Cell, alpha-beta / genetics. T-Lymphocyte Subsets / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17601376.001).
  • [ISSN] 1672-7681
  • [Journal-full-title] Cellular & molecular immunology
  • [ISO-abbreviation] Cell. Mol. Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Complementarity Determining Regions; 0 / Receptors, Antigen, T-Cell, alpha-beta
  •  go-up   go-down


55. Pawlik A, Florczak M, Ostanek L, Brzosko M, Brzosko I, Szklarz BG: TNF-alpha -308 promoter polymorphism in patients with rheumatoid arthritis. Scand J Rheumatol; 2005;34(1):22-6
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TNF-alpha -308 promoter polymorphism in patients with rheumatoid arthritis.
  • OBJECTIVES: Rheumatoid arthritis (RA) is a chronic inflammatory disease in which tumour necrosis factor-alpha (TNF-alpha) plays an important role.
  • There are, however, controversial reports that TNF-alpha promoter polymorphism may be an independent marker of susceptibility and severity of RA.
  • The aim of the present study was to examine the TNF-alpha -308 promoter polymorphism in patients with RA.
  • Polymerase chain reaction (PCR) amplification was used for analysis of the polymorphism at position -308 in promoter of TNF-alpha gene.
  • RESULTS: Distribution of TNF-alpha genotypes in RA patients did not differ from that in control subjects.
  • Moreover, there was no association between TNF-alpha genotypes and age at disease diagnosis, disease activity in global physician's assessment, and joint and extra-articular involvement.
  • There was also no correlation between TNF-alpha polymorphism and disease activity measures, including erythrocyte sedimentation rate (ESR), CRP, number of swollen and tender joints, and morning stiffness duration.
  • CONCLUSIONS: We suggest that TNF-alpha -308 promoter polymorphism is not a genetic risk factor for RA susceptibility and severity.
  • [MeSH-major] Arthritis, Rheumatoid / genetics. Polymorphism, Genetic. Promoter Regions, Genetic. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Disease Susceptibility. Female. Genetic Markers. Genotype. Humans. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Restriction Fragment Length. Severity of Illness Index


56. Kang H, Lee SK, Cho SW, Lee SH, Kwack K: Branched chain alpha-keto acid dehydrogenase, E1-beta subunit gene is associated with premature ovarian failure. Fertil Steril; 2008 Mar;89(3):728-31
MedlinePlus Health Information. consumer health - Premature Ovarian Failure.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Branched chain alpha-keto acid dehydrogenase, E1-beta subunit gene is associated with premature ovarian failure.
  • Genetic variants of the human branched chain alpha-keto acid dehydrogenase, E1-beta subunit (BCKDHB) gene were identified and they have been associated with premature ovarian failure (POF).
  • [MeSH-minor] Adult. Case-Control Studies. Female. Genetic Predisposition to Disease. Gonadotropins / blood. Haplotypes. Humans. Linkage Disequilibrium. Phenotype. Protein Subunits / genetics. Risk Factors

  • Genetic Alliance. consumer health - premature ovarian failure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17524396.001).
  • [ISSN] 1556-5653
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gonadotropins; 0 / Protein Subunits; EC 1.2.4.4 / 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)
  •  go-up   go-down


57. Kand'ár R, Záková P, Jirosová J, Sladká M: Determination of branched chain amino acids, methionine, phenylalanine, tyrosine and alpha-keto acids in plasma and dried blood samples using HPLC with fluorescence detection. Clin Chem Lab Med; 2009;47(5):565-72
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Determination of branched chain amino acids, methionine, phenylalanine, tyrosine and alpha-keto acids in plasma and dried blood samples using HPLC with fluorescence detection.
  • BACKGROUND: The determination of branched chain amino acids [BCAA; valine (Val), leucine (Leu), isoleucine (Ile)], alpha-keto acids derived from BCAA [BCKA; alpha-ketoisovaleric acid (KIV), alpha-ketoisocaproic acid (KIC), alpha-ketomethylvaleric acid (KMV)], methionine (Met), phenylalanine (Phe) and tyrosine (Tyr) is currently the most reliable approach for the diagnosis of maple syrup urine disease (MSUD), hypermethioninemia, phenylketonuria (PKU) and tyrosinemia.

  • MedlinePlus Health Information. consumer health - Amino Acid Metabolism Disorders.
  • Hazardous Substances Data Bank. L-TYROSINE .
  • Hazardous Substances Data Bank. (L)-Methionine .
  • Hazardous Substances Data Bank. (L)-Phenylalanine .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19290779.001).
  • [ISSN] 1434-6621
  • [Journal-full-title] Clinical chemistry and laboratory medicine
  • [ISO-abbreviation] Clin. Chem. Lab. Med.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Amino Acids, Branched-Chain; 0 / Keto Acids; 42HK56048U / Tyrosine; 47E5O17Y3R / Phenylalanine; AE28F7PNPL / Methionine
  •  go-up   go-down


58. Beyer K, Humbert J, Ferrer A, Lao JI, Carrato C, López D, Ferrer I, Ariza A: Low alpha-synuclein 126 mRNA levels in dementia with Lewy bodies and Alzheimer disease. Neuroreport; 2006 Aug 21;17(12):1327-30
MedlinePlus Health Information. consumer health - Lewy Body Disease.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low alpha-synuclein 126 mRNA levels in dementia with Lewy bodies and Alzheimer disease.
  • Alpha-synuclein, a main component of Lewy bodies in synucleinopathies and senile plaques in Alzheimer disease, is centrally involved in neurodegeneration.
  • Three different isoforms (alpha-synuclein 112, 126, and 140) resulting from alternative splicing have been described so far.
  • The present study explores alpha-synuclein 126 mRNA expression levels in the prefrontal cortex of six patients with dementia with Lewy bodies, eight patients with Lewy body variant of Alzheimer disease, eight patients with Alzheimer disease, and 10 controls.
  • Relative alpha-synuclein 126 expression levels were determined by real-time polymerase chain reaction with competimer technology.
  • Alpha-synuclein 126 mRNA expression was markedly decreased in the three dementias in comparison with controls, suggesting an important role of this alpha-synuclein isoform in the normal brain.
  • [MeSH-major] Alzheimer Disease / metabolism. Gene Expression Regulation / physiology. Lewy Body Disease / metabolism. Prefrontal Cortex / metabolism. RNA, Messenger / metabolism. alpha-Synuclein / metabolism
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Postmortem Changes. Protein Isoforms / genetics. Protein Isoforms / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Sequence Alignment

  • Genetic Alliance. consumer health - Alzheimer Disease.
  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16951579.001).
  • [ISSN] 0959-4965
  • [Journal-full-title] Neuroreport
  • [ISO-abbreviation] Neuroreport
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / alpha-Synuclein
  •  go-up   go-down


59. Peters IR, Helps CR, Calvert EL, Hall EJ, Day MJ: Measurement of messenger RNA encoding the alpha-chain, polymeric immunoglobulin receptor, and J-chain in duodenal mucosa from dogs with and without chronic diarrhea by use of quantitative real-time reverse transcription-polymerase chain reaction assays. Am J Vet Res; 2005 Jan;66(1):11-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Measurement of messenger RNA encoding the alpha-chain, polymeric immunoglobulin receptor, and J-chain in duodenal mucosa from dogs with and without chronic diarrhea by use of quantitative real-time reverse transcription-polymerase chain reaction assays.
  • OBJECTIVE: To examine the difference in expression of messenger RNA (mRNA) transcripts for polymeric immunoglobulin receptor (plgR), alpha-chain, and J-chain determined by use of quantitative real-time reverse transcription-polymerase chain reaction (QRT-PCR) assays in duodenal biopsy specimens obtained from dogs with and without chronic diarrhea.
  • SAMPLE POPULATION: Biopsy specimens of the proximal portion of the duodenum were obtained endoscopically from 39 dogs evaluated because of chronic diarrhea (12 German Shepherd Dogs and 27 non-German Shepherd Dog breeds); specimens were also obtained from a control group of 7 dogs evaluated because of other gastrointestinal tract diseases and 2 dogs that were euthanatized as a result of nongastrointestinal tract disease.
  • One-step QRT-PCR was used to quantify the level of expression of transcripts for the housekeeper gene glyceraldehyde-3-phosphate dehydrogenase, plgR, alpha-chain, and J-chain in duodenal mucosal tissue.
  • Conclusions and Clinical Relevance-Results indicated that the susceptibility of German Shepherd Dogs to chronic diarrhea is not a result of simple failure of transcription of the key genes that encode molecules involved in mucosal IgA secretion.
  • [MeSH-major] Diarrhea / veterinary. Dog Diseases / immunology. Immunoglobulin A, Secretory / biosynthesis. Immunoglobulin J-Chains / biosynthesis. Immunoglobulin alpha-Chains / biosynthesis. Receptors, Polymeric Immunoglobulin / biosynthesis
  • [MeSH-minor] Animals. Chronic Disease. Dogs. Duodenum / immunology. Female. Gene Expression. Intestinal Mucosa / immunology. Male. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / veterinary

  • MedlinePlus Health Information. consumer health - Diarrhea.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15691029.001).
  • [ISSN] 0002-9645
  • [Journal-full-title] American journal of veterinary research
  • [ISO-abbreviation] Am. J. Vet. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin A, Secretory; 0 / Immunoglobulin J-Chains; 0 / Immunoglobulin alpha-Chains; 0 / RNA, Messenger; 0 / Receptors, Polymeric Immunoglobulin
  •  go-up   go-down


60. Abkowitz JL, Sabo KM, Yang Z, Vite CH, Shields LE, Haskins ME: In utero transplantation of monocytic cells in cats with alpha-mannosidosis. Transplantation; 2009 Aug 15;88(3):323-9
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In utero transplantation of monocytic cells in cats with alpha-mannosidosis.
  • BACKGROUND: Lysosomal storage diseases are devastating illnesses, in large part because of their neurologic consequences.
  • METHODS: We studied the feasibility and efficacy of IU injections of monocytic cells (derived from normal marrow) in feline alpha-mannosidosis.
  • Heterozygous cats were interbred to produce affected (homozygous) and control (heterozygous and wild-type) offspring.
  • After birth, affected kittens were evaluated clinically and pathologically, tissue alpha-mannosidase levels were assayed, and in many studies, the numbers of alpha-mannosidase-containing cells were enumerated.
  • When male donor cells were transplanted into female recipients, engraftment was also quantified using polymerase chain reaction to amplify a Y chromosome-specific sequence.
  • We show that the donor monocytic cells engraft and persist (for up to 125 days) in the brain, liver, and spleen, albeit at levels below those needed to alter the clinical or pathological progression of the alpha-mannosidosis.
  • CONCLUSIONS: This is the first study of monocyte transplantation in a large animal model of a lysosomal storage disorder and demonstrates its feasibility, safety, and promise.

  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • COS Scholar Universe. author profiles.
  • SciCrunch. OMIA - Online Mendelian Inheritance in Animals: Data: Gene Expression .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2000 Jun 1;95(11):3631-3 [10828055.001]
  • [Cites] J Am Vet Med Assoc. 1986 Dec 1;189(11):1483-5 [3804848.001]
  • [Cites] Am J Pathol. 2000 Jun;156(6):1849-54 [10854208.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Aug;60(8):817-28 [11487056.001]
  • [Cites] J Pediatr. 2004 May;144(5):569-73 [15126988.001]
  • [Cites] J Gene Med. 2004 May;6(5):481-506 [15133760.001]
  • [Cites] J Inherit Metab Dis. 2004;27(3):385-410 [15190196.001]
  • [Cites] Anat Embryol (Berl). 1978 Jun 12;153(3):243-67 [677473.001]
  • [Cites] Arch Dis Child. 1987 Oct;62(10):1044-9 [3314721.001]
  • [Cites] J Inherit Metab Dis. 1988;11(1):3-16 [3128686.001]
  • [Cites] Vet Rec. 1988 Apr 9;122(15):351-4 [3381451.001]
  • [Cites] Neuroscience. 1992;48(2):405-15 [1603325.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):2970-4 [8159689.001]
  • [Cites] Lancet. 1995 Jun 3;345(8962):1398-402 [7760610.001]
  • [Cites] J Inherit Metab Dis. 1995;18(4):413-29 [7494400.001]
  • [Cites] Blood. 1997 Aug 1;90(3):986-93 [9242527.001]
  • [Cites] Stem Cells. 1998;16(4):288-93 [9708451.001]
  • [Cites] J Pediatr. 1998 Aug;133(2):282-5 [9709723.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14880-5 [9843984.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14944-9 [9843995.001]
  • [Cites] Pediatr Transplant. 1998 Nov;2(4):250-3 [10084724.001]
  • [Cites] Curr Opin Neurol. 1999 Apr;12(2):167-76 [10226749.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Sep 7;262(3):610-4 [10471372.001]
  • [Cites] Blood. 1999 Sep 15;94(6):2142-50 [10477745.001]
  • [Cites] Best Pract Res Clin Obstet Gynaecol. 2004 Dec;18(6):941-58 [15582548.001]
  • [Cites] J Med Primatol. 2005 Aug;34(4):201-8 [16053498.001]
  • [Cites] Blood. 2007 Feb 1;109(3):1331-3 [17023584.001]
  • [Cites] Biochem J. 1980 Sep 1;189(3):467-73 [7213340.001]
  • [Cites] Acta Neuropathol. 1982;58(1):64-8 [7136518.001]
  • [Cites] Acta Neuropathol. 1984;62(4):291-7 [6375239.001]
  • [Cites] Bone Marrow Transplant. 2000 May;25(10):1097-9 [10828872.001]
  • (PMID = 19667933.001).
  • [ISSN] 1534-6080
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK049652-07; United States / NIDDK NIH HHS / DK / R01 DK049652; United States / NCRR NIH HHS / RR / P40 RR002512; United States / NIDDK NIH HHS / DK / R01 DK049652-08; United States / NIDDK NIH HHS / DK / R01 DK 49652; United States / NIDDK NIH HHS / DK / DK049652-06; United States / NIDDK NIH HHS / DK / R01 DK049652-06; United States / NIDDK NIH HHS / DK / DK049652-05; United States / NIDDK NIH HHS / DK / DK049652-08; United States / NIDDK NIH HHS / DK / R01 DK049652-07; United States / NCRR NIH HHS / RR / P40 RR 02512; United States / NIDDK NIH HHS / DK / R01 DK049652-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.1.24 / alpha-Mannosidase
  • [Other-IDs] NLM/ NIHMS131484; NLM/ PMC2742773
  •  go-up   go-down


61. Etter JF, Hoda JC, Perroud N, Munafò M, Buresi C, Duret C, Neidhart E, Malafosse A, Bertrand D: Association of genes coding for the alpha-4, alpha-5, beta-2 and beta-3 subunits of nicotinic receptors with cigarette smoking and nicotine dependence. Addict Behav; 2009 Sep;34(9):772-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of genes coding for the alpha-4, alpha-5, beta-2 and beta-3 subunits of nicotinic receptors with cigarette smoking and nicotine dependence.
  • We assessed whether smoking behavior was associated with nine polymorphisms in genes coding for the nicotinic receptor subunits alpha-4 (rs1044394, rs1044396, rs2236196 and rs2273504), alpha-5 (rs16969968), beta-2 (rs2072661 and rs4845378) and beta-3 (rs4953 and rs6474413).We conducted an Internet survey and collected saliva by mail for DNA and cotinine analyses, in Switzerland in 2003.
  • [MeSH-major] Polymorphism, Single Nucleotide. Receptors, Nicotinic / genetics. Smoking / genetics. Tobacco Use Disorder / genetics
  • [MeSH-minor] Adult. Cotinine / analysis. Female. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Nerve Tissue Proteins / genetics. Polymerase Chain Reaction / methods. Polymorphism, Restriction Fragment Length. Saliva / chemistry

  • MedlinePlus Health Information. consumer health - Smoking.
  • COS Scholar Universe. author profiles.
  • Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 982006956 for PMID:19482438 [PharmGKB] .
  • Hazardous Substances Data Bank. Cotinine .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19482438.001).
  • [ISSN] 1873-6327
  • [Journal-full-title] Addictive behaviors
  • [ISO-abbreviation] Addict Behav
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CHRNA5 protein, human; 0 / CHRNB3 protein, human; 0 / Nerve Tissue Proteins; 0 / Receptors, Nicotinic; 0 / nicotinic acetylcholine receptor alpha4 subunit; 0 / nicotinic receptor beta2; K5161X06LL / Cotinine
  •  go-up   go-down


62. Déniz-Naranjo MC, Muñoz-Fernandez C, Alemany-Rodríguez MJ, Pérez-Vieitez MC, Aladro-Benito Y, Irurita-Latasa J, Sánchez-García F: Cytokine IL-1 beta but not IL-1 alpha promoter polymorphism is associated with Alzheimer disease in a population from the Canary Islands, Spain. Eur J Neurol; 2008 Oct;15(10):1080-4
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytokine IL-1 beta but not IL-1 alpha promoter polymorphism is associated with Alzheimer disease in a population from the Canary Islands, Spain.
  • AIMS: Previous studies have reported the presence of low-grade inflammation in Alzheimer disease (AD).
  • Based on these data, our work attempts to investigate the effects of some promoter polymorphisms of pro-inflammatory cytokines [interleukin (IL)-1 alpha and IL-1 beta] on AD.
  • PATIENTS AND METHODS: A PCR-RFLP technique was used to analyze the promoter polymorphisms of both IL-1 alpha (-889 C/T) and IL-1 beta (-511 C/T) and the APOE genotype from the DNA samples of 282 patients (according to NINCDS-ADRDA criteria) and 312 control subjects.
  • (ii) such risk was independent of the risk factor allele in the APOE gene (APOE4); and (iii) the IL-1 alpha promoter polymorphism (-889 C/T) was not associated with the disease.
  • [MeSH-major] Alzheimer Disease / genetics. Interleukin-1alpha / genetics. Interleukin-1beta / genetics. Polymorphism, Genetic. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. Apolipoproteins E / genetics. Case-Control Studies. DNA Mutational Analysis. Female. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Restriction Fragment Length. Spain / epidemiology

  • Genetic Alliance. consumer health - Alzheimer Disease.
  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18717723.001).
  • [ISSN] 1468-1331
  • [Journal-full-title] European journal of neurology
  • [ISO-abbreviation] Eur. J. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apolipoproteins E; 0 / Interleukin-1alpha; 0 / Interleukin-1beta
  •  go-up   go-down


63. Schroeder F, Petrescu AD, Huang H, Atshaves BP, McIntosh AL, Martin GG, Hostetler HA, Vespa A, Landrock D, Landrock KK, Payne HR, Kier AB: Role of fatty acid binding proteins and long chain fatty acids in modulating nuclear receptors and gene transcription. Lipids; 2008 Jan;43(1):1-17
Guide to Pharmacology. gene/protein/disease-specific - Fatty acid-binding proteins - overview and references .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of fatty acid binding proteins and long chain fatty acids in modulating nuclear receptors and gene transcription.
  • Abnormal energy regulation may significantly contribute to the pathogenesis of obesity, diabetes mellitus, cardiovascular disease, and cancer.
  • For longer impact, transcriptional regulation is more effective, especially in response to nutrients such as long chain fatty acids (LCFA).
  • Recent advances provide insights into how poorly water-soluble lipid nutrients [LCFA; retinoic acid (RA)] and their metabolites (long chain fatty acyl Coenzyme A, LCFA-CoA) reach nuclei, bind their cognate ligand-activated receptors, and regulate transcription for signaling lipid and glucose catabolism or storage: (i) while serum and cytoplasmic LCFA levels are in the 200 mircroM-mM range, real-time imaging recently revealed that LCFA and LCFA-CoA are also located within nuclei (nM range);.
  • (ii) sensitive fluorescence binding assays show that LCFA-activated nuclear receptors [peroxisome proliferator-activated receptor-alpha (PPARalpha) and hepatocyte nuclear factor 4alpha (HNF4alpha)] exhibit high affinity (low nM KdS) for LCFA (PPARalpha) and/or LCFA-CoA (PPARalpha, HNF4alpha)-in the same range as nuclear levels of these ligands;.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17882463.001).
  • [ISSN] 0024-4201
  • [Journal-full-title] Lipids
  • [ISO-abbreviation] Lipids
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK41402; United States / NIGMS NIH HHS / GM / P20 GM72041; United States / NIDDK NIH HHS / DK / K99 DK077573-01; United States / NIDDK NIH HHS / DK / DK077573-01; United States / NIDDK NIH HHS / DK / DK70965; United States / NIDDK NIH HHS / DK / K99 DK077573
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Fatty Acid-Binding Proteins; 0 / Fatty Acids; 0 / Ligands; 0 / Receptors, Cytoplasmic and Nuclear
  • [Number-of-references] 135
  •  go-up   go-down


64. Probert CS, Saubermann LJ, Balk S, Blumberg RS: Repertoire of the alpha beta T-cell receptor in the intestine. Immunol Rev; 2007 Feb;215:215-25
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Repertoire of the alpha beta T-cell receptor in the intestine.
  • The majority of T cells in the human and mouse intestine express the T-cell receptor (TCR) as an alphabeta heterodimer on their cell surface.
  • As the major recognition element of antigens in the context of major histocompatibility complex-derived proteins, an examination of the structure of the alpha beta TCR in intestines has provided significant insights into the potential function of these cells and the major determinants that drive their selection.
  • Studies in the human intestine have shown that the repertoires of intraepithelial lymphocytes (IELs), and likely lamina propria lymphocytes, are polyclonal before and shortly after birth, with the repertoire becoming oligoclonal in adults.
  • Studies in human inflammatory bowel disease (IBD) indicate that inflammation further skews the TCR repertoire.
  • [MeSH-major] Immunity, Mucosal. Intestinal Mucosa / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology. T-Lymphocyte Subsets / immunology
  • [MeSH-minor] Animals. Epithelial Cells / immunology. Gene Rearrangement, beta-Chain T-Cell Antigen Receptor. Humans. Inflammatory Bowel Diseases / immunology. Phenotype

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17291291.001).
  • [ISSN] 0105-2896
  • [Journal-full-title] Immunological reviews
  • [ISO-abbreviation] Immunol. Rev.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK44319; United States / NIDDK NIH HHS / DK / DK51362; United States / NIDDK NIH HHS / DK / DK53056
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, alpha-beta
  • [Number-of-references] 69
  •  go-up   go-down


65. Zhu L, Yang X, Chen W, Li X, Ji Y, Mao H, Nie J, Yu X: Decreased expressions of the TNF-alpha signaling adapters in peripheral blood mononuclear cells (PBMCs) are correlated with disease activity in patients with systemic lupus erythematosus. Clin Rheumatol; 2007 Sep;26(9):1481-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Decreased expressions of the TNF-alpha signaling adapters in peripheral blood mononuclear cells (PBMCs) are correlated with disease activity in patients with systemic lupus erythematosus.
  • Tumor necrosis factor (TNF)-alpha is a pleiotropic cytokine.
  • Systemic lupus erythematosus (SLE) is an autoimmune and inflammatory disease.
  • This study aims to investigate the expression of mRNA for the TNF adapter proteins including TNF receptor-associated death domain (TRADD) protein, Fas-associated death domain (FADD) protein, receptor-interacting protein 1 (RIP-1), and TNF receptor-associated factor-2 (TRAF-2) in peripheral blood mononuclear cells (PBMCs) from patients with SLE and to explore the relationship between the expression of these adapters and the SLE disease activity.
  • The expression of mRNA for TNF adapter molecules such as TRADD, FADD, RIP-1, and TRAF-2 in PBMCs were analyzed by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) and quantitative real-time RT-PCR.
  • These abnormalities may be involved in the immunopathogenic injury mediated by the aberration TNF-alpha signaling pathway in SLE.
  • [MeSH-major] Leukocytes, Mononuclear / metabolism. Lupus Erythematosus, Systemic / physiopathology. Tumor Necrosis Factor-alpha / metabolism

  • Genetic Alliance. consumer health - Lupus.
  • Genetic Alliance. consumer health - Systemic lupus erythematosus.
  • MedlinePlus Health Information. consumer health - Lupus.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17235653.001).
  • [ISSN] 0770-3198
  • [Journal-full-title] Clinical rheumatology
  • [ISO-abbreviation] Clin. Rheumatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / FADD protein, human; 0 / Fas-Associated Death Domain Protein; 0 / TNF Receptor-Associated Death Domain Protein; 0 / TNF Receptor-Associated Factor 2; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.1 / Receptor-Interacting Protein Serine-Threonine Kinases; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


66. Taylor KN, Shinde Patil VR, Colson YL: Reconstitution of allogeneic hemopoietic stem cells: the essential role of FcR gamma and the TCR beta-chain-FCp33 complex. J Immunol; 2006 Aug 1;177(3):1444-50
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reconstitution of allogeneic hemopoietic stem cells: the essential role of FcR gamma and the TCR beta-chain-FCp33 complex.
  • Transplantation of purified allogeneic hemopoietic stem cells (SC) alone is characterized by a decreased risk of graft-vs-host disease but increased incidence of engraftment failure.
  • It has been established that the facilitating cell (FC) promotes allogeneic SC reconstitution and results in donor-specific transplantation tolerance across MHC disparities, without graft-vs-host disease.
  • Although the requirements for this facilitating function are not well-characterized, it is known that facilitation is dependent on FC expression of a unique heterodimer consisting of the TCR beta-chain (TCRbeta) and a 33-kDa protein, FCp33.
  • [MeSH-major] Bone Marrow Transplantation / immunology. Carrier Proteins / physiology. Hematopoietic Stem Cell Transplantation. Isoantigens / metabolism. Receptors, Antigen, T-Cell, alpha-beta / physiology. Receptors, IgG / physiology

  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16849450.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL074150-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Carrier Proteins; 0 / Cd3e protein, mouse; 0 / FCp33 protein, mouse; 0 / Isoantigens; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, IgG
  •  go-up   go-down


67. Ye D, Ma I, Ma TY: Molecular mechanism of tumor necrosis factor-alpha modulation of intestinal epithelial tight junction barrier. Am J Physiol Gastrointest Liver Physiol; 2006 Mar;290(3):G496-504
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular mechanism of tumor necrosis factor-alpha modulation of intestinal epithelial tight junction barrier.
  • A TNF-alpha-induced increase in intestinal epithelial tight junction (TJ) permeability has been proposed to be an important proinflammatory mechanism contributing to intestinal inflammation in Crohn's disease and other inflammatory conditions.
  • Previous studies from our laboratory suggested that the TNF-alpha-induced increase in intestinal TJ permeability was mediated by an increase in myosin light chain kinase (MLCK) protein expression.
  • However, the molecular mechanisms that mediate the TNF-alpha increase in intestinal TJ permeability and MLCK protein expression remain unknown.
  • The purpose of this study was to delineate the intracellular and molecular mechanisms that mediate the TNF-alpha-induced increase in intestinal TJ permeability; using an in vitro intestinal epithelial model system consisting of filter-grown Caco-2 intestinal epithelial monolayers.
  • To examine the molecular mechanisms involved in the TNF-alpha regulation of intestinal TJ barrier, we identified and cloned for the first time a functionally active MLCK promoter region.
  • TNF-alpha treatment of filter-grown Caco-2 monolayers transfected with plasmid vector containing the MLCK promoter region produced an increase in MLCK promoter activity and MLCK transcription.
  • The TNF-alpha-induced increase in MLCK transcription corresponded to a sequential increase in MLCK protein expression, MLCK activity, and Caco-2 TJ permeability.
  • The TNF-alpha-induced increase in MLCK promoter activity was mediated by NF-kappaB activation, and the inhibition of NF-kappaB activation prevented the TNF-alpha-induced increase in promoter activity and the subsequent increase in MLCK protein expression and Caco-2 TJ permeability.
  • The TNF-alpha-induced activation of MLCK promoter was mediated by binding of the activated NF-kappaB p50/p65 dimer to the downstream kappaB binding site (-84 to -75) on the MLCK promoter region; deletion of the kappaB binding site prevented the TNF-alpha increase in promoter activity.
  • Additionally, siRNA silencing of NF-kappaB p65 also prevented the TNF-alpha increase in MLCK promoter activity.
  • In conclusion, our findings indicated that the TNF-alpha-induced increase in intestinal epithelial TJ permeability was mediated by NF-kappaB p50/p65 binding and activation of the MLCK promoter.
  • NF-kappaB p50/p65 activation of the MLCK promoter then leads to a stepwise increase in MLCK transcription, expression and activity, and MLCK-mediated opening of the intestinal TJ barrier.
  • [MeSH-major] Tight Junctions / physiology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Caco-2 Cells. Cell Membrane Permeability / drug effects. Cell Membrane Permeability / physiology. Curcumin / pharmacology. Humans. I-kappa B Proteins / metabolism. Myosin-Light-Chain Kinase / biosynthesis. NF-kappa B / antagonists & inhibitors. NF-kappa B / pharmacology. Promoter Regions, Genetic / drug effects. Pyrrolidines / pharmacology. RNA Interference. Thiocarbamates / pharmacology. Up-Regulation

  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • Hazardous Substances Data Bank. CURCUMIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16474009.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01-DK-64165-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Pyrrolidines; 0 / Thiocarbamates; 0 / Tumor Necrosis Factor-alpha; 25769-03-3 / pyrrolidine dithiocarbamic acid; EC 2.7.11.18 / Myosin-Light-Chain Kinase; IT942ZTH98 / Curcumin
  •  go-up   go-down


68. Stauber AJ, Brown-Borg H, Liu J, Waalkes MP, Laughter A, Staben RA, Coley JC, Swanson C, Voss KA, Kopchick JJ, Corton JC: Constitutive expression of peroxisome proliferator-activated receptor alpha-regulated genes in dwarf mice. Mol Pharmacol; 2005 Mar;67(3):681-94
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Constitutive expression of peroxisome proliferator-activated receptor alpha-regulated genes in dwarf mice.
  • Defects in growth hormone secretion or signaling in mice are associated with decreased body weights (dwarfism), increased longevity, increased resistance to stress, and decreases in factors that contribute to cardiovascular disease and cancer.
  • Peroxisome proliferators (PP) alter a subset of these changes in wild-type mice through activation of the nuclear receptor family member PP-activated receptor alpha (PPARalpha).
  • We tested the hypothesis that an overlap in the transcriptional programs between untreated dwarf mice and PP-treated wild-type mice underlies these similarities.
  • The genes included those involved in beta- and omega-oxidation of fatty acids (Acox1, Cyp4a10, Cyp4a14) and those involved in stress responses (the chaperonin, T-complex protein1epsilon) and cardiovascular disease (fibrinogen).
  • [MeSH-major] Dwarfism / genetics. Gene Expression Regulation / physiology. PPAR alpha / physiology
  • [MeSH-minor] Animals. Base Sequence. DNA Primers. Mice. Mice, Knockout. Mice, Mutant Strains. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Dwarfism.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15576629.001).
  • [ISSN] 0026-895X
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / PPAR alpha
  •  go-up   go-down


69. Maguire-Zeiss KA, Wang CI, Yehling E, Sullivan MA, Short DW, Su X, Gouzer G, Henricksen LA, Wuertzer CA, Federoff HJ: Identification of human alpha-synuclein specific single chain antibodies. Biochem Biophys Res Commun; 2006 Nov 3;349(4):1198-205
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of human alpha-synuclein specific single chain antibodies.
  • Parkinson's disease (PD) is a common neurodegenerative disease of unknown etiology.
  • Evidence suggests a role for protein misfolding in disease pathogenesis.
  • One component of Lewy bodies, the presynaptic protein, alpha-synuclein forms oligomers and higher order aggregates and is proposed to be involved in dopaminergic neuronal death.
  • In an effort to discriminate between alpha-synuclein conformational forms as well as design potential disruptors of pathogenic misfolding we panned a human phage antibody library for anti-synuclein single chain antibodies (scFvs).
  • We identified six scFvs which recognize different conformers of alpha-synuclein in both an ELISA and Western blot analysis.
  • These scFvs may further our understanding of alpha-synuclein's role in PD.
  • [MeSH-major] Immunoglobulin Variable Region / chemistry. Immunoglobulin Variable Region / immunology. alpha-Synuclein / chemistry. alpha-Synuclein / immunology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16973126.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Variable Region; 0 / alpha-Synuclein
  •  go-up   go-down


70. Gawlik KI, Akerlund M, Carmignac V, Elamaa H, Durbeej M: Distinct roles for laminin globular domains in laminin alpha1 chain mediated rescue of murine laminin alpha2 chain deficiency. PLoS One; 2010;5(7):e11549
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct roles for laminin globular domains in laminin alpha1 chain mediated rescue of murine laminin alpha2 chain deficiency.
  • BACKGROUND: Laminin alpha2 chain mutations cause congenital muscular dystrophy with dysmyelination neuropathy (MDC1A).
  • Previously, we demonstrated that laminin alpha1 chain ameliorates the disease in mice.
  • Unlike laminin alpha2 chain, alpha1 chain binds the receptors by separate domains; laminin globular (LG) domains 4 and LG1-3, respectively.
  • Thus, the laminin alpha1 chain is an excellent tool to distinguish between the roles of dystroglycan and integrins in the neuromuscular system.
  • Overexpression of laminin alpha1 chain that lacks the dystroglycan binding LG4-5 domains in alpha2 chain deficient mice resulted in prolonged lifespan and improved health.
  • [MeSH-minor] Animals. Antigens, CD / genetics. Antigens, CD / metabolism. Basement Membrane / metabolism. Basement Membrane / pathology. Body Weight / physiology. Creatine Kinase / metabolism. Dystroglycans / genetics. Dystroglycans / metabolism. Immunoblotting. Integrin alpha Chains / genetics. Integrin alpha Chains / metabolism. Locomotion / physiology. Mice. Mice, Transgenic. Microscopy, Electron, Transmission. Microscopy, Fluorescence. Muscle, Skeletal / metabolism. Muscle, Skeletal / pathology. Myelin Sheath / metabolism. Peripheral Nervous System / metabolism. Peripheral Nervous System / pathology. Protein Structure, Tertiary / genetics. Protein Structure, Tertiary / physiology

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Cell Biol. 2005 Feb 14;168(4):655-66 [15699217.001]
  • [Cites] J Cell Biol. 2005 Apr 11;169(1):179-89 [15824137.001]
  • [Cites] FASEB J. 2005 Jun;19(8):934-42 [15923403.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 23;102(34):11999-2004 [16103356.001]
  • [Cites] Am J Pathol. 2005 Sep;167(3):823-33 [16127160.001]
  • [Cites] J Cell Sci. 2006 Jan 15;119(Pt 2):199-207 [16410545.001]
  • [Cites] Glia. 2006 Mar;53(4):372-81 [16288467.001]
  • [Cites] Hum Mol Genet. 2006 Mar 15;15(6):989-98 [16476707.001]
  • [Cites] FEBS Lett. 2006 Mar 20;580(7):1759-65 [16504180.001]
  • [Cites] Matrix Biol. 2006 Apr;25(3):189-97 [16413178.001]
  • [Cites] Hum Mol Genet. 2006 Sep 15;15(18):2690-700 [16893907.001]
  • [Cites] Int J Biochem Cell Biol. 2007;39(3):505-28 [17097330.001]
  • [Cites] J Cell Biol. 2007 Mar 26;176(7):979-93 [17389231.001]
  • [Cites] Nat Genet. 1999 Nov;23(3):338-42 [10610181.001]
  • [Cites] Trends Biotechnol. 2007 Jun;25(6):262-8 [17416431.001]
  • [Cites] J Biol Chem. 2007 Jul 20;282(29):21437-47 [17517882.001]
  • [Cites] J Mol Biol. 2007 Aug 31;371(5):1188-203 [17618648.001]
  • [Cites] Microsc Res Tech. 2008 May;71(5):349-56 [18219670.001]
  • [Cites] J Neurosci. 2008 Jun 25;28(26):6714-9 [18579745.001]
  • [Cites] J Neurosci. 2008 Oct 15;28(42):10567-75 [18923033.001]
  • [Cites] J Cell Sci. 2009 Jan 15;122(Pt 2):289-99 [19118221.001]
  • [Cites] Am J Pathol. 2009 Jan;174(1):256-64 [19074617.001]
  • [Cites] Ann Neurol. 2009 Jan;65(1):47-56 [19086074.001]
  • [Cites] J Biol Chem. 2009 Mar 27;284(13):8984-94 [19189961.001]
  • [Cites] Hum Mol Genet. 2004 Aug 15;13(16):1775-84 [15213105.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):12573-9 [19633189.001]
  • [Cites] Brain Pathol. 2009 Oct;19(4):596-611 [18691338.001]
  • [Cites] Muscle Nerve. 2010 Jul;42(1):30-7 [20544910.001]
  • [Cites] Muscle Nerve. 2002 Nov;26(5):644-53 [12402286.001]
  • [Cites] J Biol Chem. 2003 Apr 25;278(17):14587-90 [12556453.001]
  • [Cites] Neuron. 2003 Jun 5;38(5):747-58 [12797959.001]
  • [Cites] Mol Cell Neurosci. 2003 Jun;23(2):210-8 [12812754.001]
  • [Cites] J Neurosci. 2003 Jul 2;23(13):5520-30 [12843252.001]
  • [Cites] J Mol Biol. 2003 Sep 19;332(3):635-42 [12963372.001]
  • [Cites] Biochemistry. 2003 Nov 4;42(43):12625-33 [14580209.001]
  • [Cites] J Cell Sci. 2004 Feb 15;117(Pt 5):735-42 [14734655.001]
  • [Cites] Muscle Nerve. 2004 Feb;29(2):292-9 [14755496.001]
  • [Cites] BMC Neurosci. 2003 Nov 18;4:29 [14622446.001]
  • [Cites] Curr Biol. 1999 Nov 18;9(22):1327-30 [10574769.001]
  • [Cites] J Cell Sci. 2004 Aug 1;117(Pt 17):3821-30 [15252120.001]
  • [Cites] Neuromuscul Disord. 2004 Oct;14(10):675-82 [15351425.001]
  • [Cites] Neuropathol Appl Neurobiol. 1979 Mar-Apr;5(2):133-47 [471185.001]
  • [Cites] J Comp Neurol. 1986 Apr 1;246(1):32-69 [3700717.001]
  • [Cites] J Cell Biol. 1990 Sep;111(3):1265-73 [2144001.001]
  • [Cites] Development. 1990 May;109(1):105-16 [2170096.001]
  • [Cites] J Cell Biol. 1992 May;117(3):671-8 [1533398.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jun 7;91(12):5572-6 [8202529.001]
  • [Cites] Hum Mol Genet. 1995 Jun;4(6):1055-61 [7655459.001]
  • [Cites] J Child Neurol. 1995 Nov;10(6):472-5 [8576559.001]
  • [Cites] J Clin Invest. 1997 Oct 1;100(7):1870-81 [9312189.001]
  • [Cites] FEBS Lett. 1997 Sep 22;415(1):33-9 [9326364.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2000 Apr;68(4):483-8 [10727485.001]
  • [Cites] EMBO J. 2000 Apr 3;19(7):1432-40 [10747011.001]
  • [Cites] J Cell Biol. 2001 Mar 19;152(6):1207-18 [11257121.001]
  • [Cites] Neuromuscul Disord. 2001 May;11(4):350-9 [11369186.001]
  • [Cites] Glia. 2001 Aug;35(2):101-10 [11460266.001]
  • [Cites] Nature. 2001 Sep 20;413(6853):302-7 [11565031.001]
  • [Cites] J Cell Biol. 2002 Jan 7;156(1):199-209 [11777940.001]
  • [Cites] J Biol Chem. 2002 Feb 22;277(8):6012-6 [11744715.001]
  • [Cites] J Cell Sci. 2002 Mar 1;115(Pt 5):1005-15 [11870219.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Apr 2;99(7):4227-32 [11917099.001]
  • [Cites] J Biol Chem. 2002 May 24;277(21):18928-37 [11886875.001]
  • [Cites] Curr Opin Genet Dev. 2002 Jun;12(3):349-61 [12076680.001]
  • [Cites] J Cell Biol. 2002 Jun 24;157(7):1279-90 [12082085.001]
  • [Cites] Cell. 2002 Sep 6;110(5):639-48 [12230980.001]
  • [Cites] J Biol Chem. 2007 Apr 13;282(15):11573-81 [17307732.001]
  • [Cites] J Cell Biol. 1997 Oct 20;139(2):375-85 [9334342.001]
  • [Cites] J Cell Biol. 1997 Dec 15;139(6):1507-21 [9396756.001]
  • [Cites] J Clin Invest. 1998 Aug 15;102(4):844-52 [9710454.001]
  • [Cites] Exp Cell Res. 1999 Jan 10;246(1):165-82 [9882526.001]
  • [Cites] EMBO J. 1999 Feb 15;18(4):863-70 [10022829.001]
  • [Cites] J Mol Biol. 1999 Mar 26;287(2):253-64 [10080889.001]
  • [Cites] J Clin Invest. 1999 Apr;103(8):1127-34 [10207164.001]
  • [Cites] J Neurol Sci. 1999 Mar 1;163(2):140-52 [10371075.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Jun 24;260(1):139-42 [10381357.001]
  • [Cites] J Neurocytol. 1998 Sep;27(9):649-59 [10447239.001]
  • [Cites] J Clin Invest. 2004 Dec;114(11):1635-9 [15578095.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Feb 1;102(5):1502-6 [15668394.001]
  • (PMID = 20657839.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Integrin alpha Chains; 0 / Laminin; 0 / integrin alpha7; 0 / laminin alpha 2; 146888-27-9 / Dystroglycans; 151186-83-3 / laminin A; EC 2.7.3.2 / Creatine Kinase
  • [Other-IDs] NLM/ PMC2906511
  •  go-up   go-down


71. Stangou AJ, Banner NR, Hendry BM, Rela M, Portmann B, Wendon J, Monaghan M, Maccarthy P, Buxton-Thomas M, Mathias CJ, Liepnieks JJ, O'Grady J, Heaton ND, Benson MD: Hereditary fibrinogen A alpha-chain amyloidosis: phenotypic characterization of a systemic disease and the role of liver transplantation. Blood; 2010 Apr 15;115(15):2998-3007
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hereditary fibrinogen A alpha-chain amyloidosis: phenotypic characterization of a systemic disease and the role of liver transplantation.
  • Variants of fibrinogen A alpha-chain (AFib) cause the most common type of hereditary renal amyloidosis in Europe and, possibly, the United States as well.
  • We assessed 22 AFib patients for combined liver and kidney transplantation (LKT) and report the clinical features and outcome.
  • Fibrinogen amyloidosis is a systemic amyloid disease with visceral, vascular, cardiac, and neurologic involvement.
  • [MeSH-minor] Adult. Cardiomyopathy, Dilated / complications. Cardiomyopathy, Dilated / pathology. Cardiomyopathy, Dilated / ultrasonography. Cardiovascular System / pathology. Female. Humans. Kidney Transplantation / radionuclide imaging. Male. Middle Aged. Mutation / genetics. Nervous System Diseases / complications. Nervous System Diseases / pathology. Patient Selection. Phenotype. Technetium Tc 99m Dimercaptosuccinic Acid. Treatment Outcome


72. Kanekura T, Sakuraba H, Matsuzawa F, Aikawa S, Doi H, Hirabayashi Y, Yoshii N, Fukushige T, Kanzaki T: Three dimensional structural studies of alpha-N-acetylgalactosaminidase (alpha-NAGA) in alpha-NAGA deficiency (Kanzaki disease): different gene mutations cause peculiar structural changes in alpha-NAGAs resulting in different substrate specificities and clinical phenotypes. J Dermatol Sci; 2005 Jan;37(1):15-20
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Three dimensional structural studies of alpha-N-acetylgalactosaminidase (alpha-NAGA) in alpha-NAGA deficiency (Kanzaki disease): different gene mutations cause peculiar structural changes in alpha-NAGAs resulting in different substrate specificities and clinical phenotypes.
  • BACKGROUND: Kanzaki disease (OMIM#104170) is attributable to a deficiency in alpha-N-acetylgalactosaminidase (alpha-NAGA; E.C.3.2.1.49), which hydrolyzes GalNAcalpha1-O-Ser/Thr.
  • Although they are on the same codon, the clinical manifestation was more severe in R329W because an amino acid substitution led to protein instability resulting in structural change, which is greater in R329W than in R329Q.
  • OBJECTIVE: To examine whether the different clinical phenotypes are attributable to the two mutations.
  • METHODS: Plasma alpha-NAGA activity and urinary excreted glycopeptides were measured and three-dimensional models of human alpha-NAGA and its complexes with GalNAcalpha1-O-Ser and GalNAcalpha1-O-Thr were constructed by homology modeling.
  • GalNAcalpha1-O-Ser/Thr fit tightly in a narrow space of the active site pocket of alpha-NAGA.
  • GalNAcalpha1-O-Thr requires a larger space to associate with alpha-NAGA because of the side chain (CH3) of the threonine residue.
  • CONCLUSION: Our findings suggest that the association of alpha-NAGA with its substrates is strongly affected by the amino acid substitution at R329 and that the association with GalNAcalpha1-O-Thr is more highly susceptible to structural changes.
  • Therefore, the urinary ratio of GalNAcalpha1-O-Ser:GalNAcalpha1-O-Thr was lower and the clinical phenotype was milder in the R329Q mutation.
  • [MeSH-major] alpha-N-Acetylgalactosaminidase / chemistry. alpha-N-Acetylgalactosaminidase / genetics


73. Deitiker PR, Oshima M, Smith RG, Mosier DR, Atassi MZ: Subtle differences in HLA DQ haplotype-associated presentation of AChR alpha-chain peptides may suffice to mediate myasthenia gravis. Autoimmunity; 2006 Jun;39(4):277-88
Immune Epitope Database and Analysis Resource. gene/protein/disease-specific - Related Immune Epitope Information .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subtle differences in HLA DQ haplotype-associated presentation of AChR alpha-chain peptides may suffice to mediate myasthenia gravis.
  • The HLA DQA1 and DQB1 alleles were determined on a set of 24 myasthenia gravis patients that had previously been examined for their T-cell proliferative responses to the 18 overlapping peptides representing the extracellular domain of hAChR alpha-chain.
  • Differences in the age of disease onset relative to DQ haplotypes were also observed.
  • Groups of A1*0301:B1*0302, A1*0501:B1*0201 and A1*0102:B1*0604 showed earlier ages of disease onset relative to those of A1*0102:B1*0602 or A1*0505:B1*0301.
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Alleles. Amino Acid Sequence. Female. Genotype. HLA-DQ alpha-Chains. HLA-DQ beta-Chains. Haplotypes. Humans. Lymphocyte Activation. Male. Middle Aged. Molecular Sequence Data. Protein Subunits / immunology

  • Genetic Alliance. consumer health - Myasthenia gravis.
  • MedlinePlus Health Information. consumer health - Myasthenia Gravis.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16891216.001).
  • [ISSN] 0891-6934
  • [Journal-full-title] Autoimmunity
  • [ISO-abbreviation] Autoimmunity
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-DQ Antigens; 0 / HLA-DQ alpha-Chains; 0 / HLA-DQ beta-Chains; 0 / HLA-DQA1 antigen; 0 / HLA-DQB1 antigen; 0 / Membrane Glycoproteins; 0 / Protein Subunits; 0 / Receptors, Cholinergic
  •  go-up   go-down


74. Lowey S, Lesko LM, Rovner AS, Hodges AR, White SL, Low RB, Rincon M, Gulick J, Robbins J: Functional effects of the hypertrophic cardiomyopathy R403Q mutation are different in an alpha- or beta-myosin heavy chain backbone. J Biol Chem; 2008 Jul 18;283(29):20579-89
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional effects of the hypertrophic cardiomyopathy R403Q mutation are different in an alpha- or beta-myosin heavy chain backbone.
  • The R403Q mutation in the beta-myosin heavy chain (MHC) was the first mutation to be linked to familial hypertrophic cardiomyopathy (FHC), a primary disease of heart muscle.
  • The introduction of the mouse model for FHC (the mouse expresses predominantly alpha-MHC as opposed to the beta-isoform in larger mammals) created a new paradigm for FHC based on finding enhanced motor function for R403Q alpha-MHC.
  • To help resolve these conflicting mechanisms, we used a transgenic mouse model in which the endogenous alpha-MHC was largely replaced with transgenically encoded beta-MHC.
  • A His(6) tag was cloned at the N terminus of the alpha-and beta-MHC to facilitate protein isolation by Ni(2+)-chelating chromatography.
  • Characterization of the R403Q alpha-MHC by the in vitro motility assay showed a 30-40% increase in actin filament velocity compared with wild type, consistent with published studies.
  • We find that the actin-activated MgATPase activity for R403Q alpha-S1 is approximately 30% higher than for wild type, whereas the enzymatic activity for R403Q beta-S1 is reduced by approximately 10%.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PROPYL THIOURACIL .
  • Hazardous Substances Data Bank. (L)-ARGININE .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochemistry. 2004 Nov 30;43(47):15058-65 [15554713.001]
  • [Cites] Circ Res. 1999 Mar 5;84(4):475-83 [10066683.001]
  • [Cites] Heart Fail Rev. 2005 Sep;10(3):237-48 [16416046.001]
  • [Cites] J Cell Biol. 2007 Apr 9;177(1):7-11 [17420288.001]
  • [Cites] J Clin Invest. 1999 Dec;104(12):1683-92 [10606622.001]
  • [Cites] Circ Res. 2000 Apr 14;86(7):737-44 [10764406.001]
  • [Cites] J Biol Chem. 2000 Sep 8;275(36):28045-52 [10882745.001]
  • [Cites] Nat Struct Biol. 2000 Dec;7(12):1147-55 [11101898.001]
  • [Cites] Methods. 2000 Dec;22(4):327-35 [11133239.001]
  • [Cites] J Muscle Res Cell Motil. 2000;21(7):609-20 [11227787.001]
  • [Cites] Cell. 2001 Feb 23;104(4):557-67 [11239412.001]
  • [Cites] J Mol Cell Cardiol. 2001 Apr;33(4):655-70 [11273720.001]
  • [Cites] J Biol Chem. 2001 Feb 9;276(6):4409-15 [11076938.001]
  • [Cites] Cell Motil Cytoskeleton. 2002 Jan;51(1):1-15 [11810692.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2002 Oct;283(4):H1446-54 [12234796.001]
  • [Cites] Trends Cardiovasc Med. 2002 Nov;12(8):348-54 [12536121.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Mar 18;100(6):3227-32 [12612343.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2007 Jul;293(1):H284-91 [17351073.001]
  • [Cites] J Biol Chem. 2007 Aug 17;282(33):24057-64 [17575272.001]
  • [Cites] PLoS One. 2007;2(11):e1123 [17987111.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2008 Apr;294(4):H1939-47 [18281382.001]
  • [Cites] J Biol Chem. 2003 May 9;278(19):17466-74 [12626511.001]
  • [Cites] J Biol Chem. 2003 Jul 18;278(29):26938-45 [12709440.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2004 Jul;287(1):H91-9 [15001446.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 27;101(30):10973-8 [15256600.001]
  • [Cites] J Gen Physiol. 1967 Jul;50(6):Suppl:197-218 [4227924.001]
  • [Cites] Eur J Biochem. 1979 Sep;99(2):385-94 [159176.001]
  • [Cites] Methods Enzymol. 1982;85 Pt B:164-81 [7121269.001]
  • [Cites] J Biol Chem. 1984 Sep 25;259(18):11226-30 [6147352.001]
  • [Cites] J Mol Biol. 1989 Dec 5;210(3):665-71 [2614840.001]
  • [Cites] Cell. 1990 Sep 7;62(5):999-1006 [1975517.001]
  • [Cites] Anal Biochem. 1992 May 1;202(2):275-85 [1519753.001]
  • [Cites] J Clin Invest. 1993 Jun;91(6):2861-5 [8514894.001]
  • [Cites] J Biol Chem. 1994 Jan 21;269(3):1603-5 [8294404.001]
  • [Cites] J Clin Invest. 1995 Mar;95(3):1409-14 [7883988.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):21-6 [8552606.001]
  • [Cites] Science. 1996 May 3;272(5262):731-4 [8614836.001]
  • [Cites] J Cell Biol. 1996 Aug;134(4):895-909 [8769415.001]
  • [Cites] J Clin Invest. 1996 Oct 15;98(8):1906-17 [8878443.001]
  • [Cites] J Clin Invest. 1996 Dec 15;98(12):2866-73 [8981935.001]
  • [Cites] J Clin Invest. 1997 Mar 1;99(5):1010-5 [9062359.001]
  • [Cites] J Mol Cell Cardiol. 1997 Feb;29(2):667-76 [9140824.001]
  • [Cites] J Muscle Res Cell Motil. 1997 Jun;18(3):275-83 [9172070.001]
  • [Cites] Cell. 1998 Sep 4;94(5):559-71 [9741621.001]
  • [Cites] Biophys J. 1998 Dec;75(6):3023-30 [9826622.001]
  • [Cites] Mol Cell. 2005 Sep 2;19(5):595-605 [16137617.001]
  • (PMID = 18480046.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL 087862; United States / NHLBI NIH HHS / HL / HL 077101; United States / NHLBI NIH HHS / HL / HL 074728; United States / NHLBI NIH HHS / HL / HL 69799; United States / NCRR NIH HHS / RR / P20 RR 16435; United States / NHLBI NIH HHS / HL / HL 59408; United States / NIAMS NIH HHS / AR / AR 053975
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 721M9407IY / Propylthiouracil; 94ZLA3W45F / Arginine; EC 3.6.1.- / Ca(2+) Mg(2+)-ATPase; EC 3.6.1.- / Ventricular Myosins; EC 3.6.4.1 / Myosin Heavy Chains
  • [Other-IDs] NLM/ PMC2459289
  •  go-up   go-down


75. Shamim Z, Müller K, Svejgaard A, Poulsen LK, Bodtger U, Ryder LP: Association between genetic polymorphisms in the human interleukin-7 receptor alpha-chain and inhalation allergy. Int J Immunogenet; 2007 Jun;34(3):149-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association between genetic polymorphisms in the human interleukin-7 receptor alpha-chain and inhalation allergy.
  • Thymic stromal-derived lymphopoietin (TSLP) and interleukin-7 share a common receptor chain, IL-7Ralpha.
  • The gene encoding the IL-7Ralpha chain is polymorphic, and investigation of inhalation allergic patients compared with controls showed significant association with two alleles at position +1237 and +2087.
  • [MeSH-minor] Adult. Case-Control Studies. Denmark / epidemiology. Female. Gene Frequency. Genetic Predisposition to Disease. Humans. Male. Middle Aged. Polymorphism, Single Nucleotide

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17504502.001).
  • [ISSN] 1744-3121
  • [Journal-full-title] International journal of immunogenetics
  • [ISO-abbreviation] Int. J. Immunogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Interleukin-7; 0 / interleukin-7 receptor, alpha chain
  •  go-up   go-down


76. Otani T, Yamaguchi K, Scherl E, Du B, Tai HH, Greifer M, Petrovic L, Daikoku T, Dey SK, Subbaramaiah K, Dannenberg AJ: Levels of NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase are reduced in inflammatory bowel disease: evidence for involvement of TNF-alpha. Am J Physiol Gastrointest Liver Physiol; 2006 Feb;290(2):G361-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Levels of NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase are reduced in inflammatory bowel disease: evidence for involvement of TNF-alpha.
  • Increased amounts of PGE(2) have been detected in the inflamed mucosa of patients with inflammatory bowel disease (IBD).
  • Amounts of 15-PGDH protein and mRNA were markedly reduced in inflamed mucosa from patients with Crohn's disease and ulcerative colitis.
  • Because of the importance of TNF-alpha in IBD, we also determined the effects of TNF-alpha on the expression of 15-PGDH in vitro.
  • Treatment with TNF-alpha suppressed the transcription of 15-PGDH in human colonocytes, resulting in reduced amounts of 15-PGDH mRNA and protein and enzyme activity.
  • In contrast, TNF-alpha induced two enzymes (cyclooxygenase-2 and microsomal prostaglandin E synthase-1) that contribute to increased synthesis of PGE(2).
  • Overexpressing 15-PGDH blocked the increase in PGE(2) production mediated by TNF-alpha.
  • The decrease in amounts of 15-PGDH in inflamed mucosa can be explained at least, in part, by TNF-alpha-mediated suppression of 15-PGDH transcription.
  • [MeSH-major] Hydroxyprostaglandin Dehydrogenases / metabolism. Inflammatory Bowel Diseases / enzymology. NAD / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Colon / cytology. Colon / metabolism. Crohn Disease / metabolism. Crohn Disease / pathology. Cyclooxygenase 2 / biosynthesis. Dinoprostone / metabolism. Gene Expression Regulation, Enzymologic / drug effects. HT29 Cells. Humans. In Situ Hybridization. Intestinal Mucosa / enzymology. Intestinal Mucosa / metabolism. RNA, Messenger / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Transfection

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16195422.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA-77839; United States / NCI NIH HHS / CA / R01 CA-111469
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 0U46U6E8UK / NAD; EC 1.1.1.- / Hydroxyprostaglandin Dehydrogenases; EC 1.1.1.141 / 15-hydroxyprostaglandin dehydrogenase; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone
  •  go-up   go-down


77. Adam-Vizi V: Production of reactive oxygen species in brain mitochondria: contribution by electron transport chain and non-electron transport chain sources. Antioxid Redox Signal; 2005 Sep-Oct;7(9-10):1140-9
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Production of reactive oxygen species in brain mitochondria: contribution by electron transport chain and non-electron transport chain sources.
  • Overwhelming evidence has accumulated indicating that oxidative stress is a crucial factor in the pathogenesis of neurodegenerative diseases.
  • The major site of production of superoxide, the primary reactive oxygen species (ROS), is considered to be the respiratory chain in the mitochondria, but the exact mechanism and the precise location of the physiologically relevant ROS generation within the respiratory chain have not been disclosed as yet.
  • In contrast, complex I inhibition to a small degree is sufficient to enhance ROS generation, indicating that inhibition of complex I by approximately 25-30% observed in postmortem samples of substantia nigra from patients suffering from Parkinson's disease could be important in inducing oxidative stress.
  • Recently, it has been described that a key Krebs cycle enzyme, alpha-ketoglutarate dehydrogenase (alpha-KGDH), is also able to produce ROS.
  • ROS formation by alpha-KGDH is regulated by the NADH/NAD+ ratio, suggesting that this enzyme could substantially contribute to generation of oxidative stress due to inhibition of complex I.
  • As alpha-KGDH is not only a generator but also a target of ROS, it is proposed that alpha-KGDH is a key factor in a vicious cycle by which oxidative stress is induced and promoted in nerve terminals.
  • [MeSH-major] Brain / pathology. Electron Transport Chain Complex Proteins / metabolism. Gene Expression Regulation, Enzymologic. Mitochondria / pathology. Reactive Oxygen Species

  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16115017.001).
  • [ISSN] 1523-0864
  • [Journal-full-title] Antioxidants & redox signaling
  • [ISO-abbreviation] Antioxid. Redox Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Electron Transport Chain Complex Proteins; 0 / Reactive Oxygen Species; 11062-77-4 / Superoxides; 6384-92-5 / N-Methylaspartate; BBX060AN9V / Hydrogen Peroxide; EC 1.15.1.1 / Superoxide Dismutase; EC 1.2.4.2 / Ketoglutarate Dehydrogenase Complex
  • [Number-of-references] 111
  •  go-up   go-down


78. Lai MI, Garner C, Jiang J, Silver N, Best S, Menzel S, Thein SL: A twins heritability study on alpha hemoglobin stabilizing protein (AHSP) expression variability. Twin Res Hum Genet; 2010 Dec;13(6):567-72
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A twins heritability study on alpha hemoglobin stabilizing protein (AHSP) expression variability.
  • Alpha hemoglobin stabilizing protein (AHSP) was found to bind only to free α-globin monomers creating a stable and inert complex which remains soluble in the cytoplasm thus preventing harmful precipitations.
  • Alpha hemoglobin stabilizing protein was shown to bind nascent α-globin monomers with transient strength before transferring α-globin to β-globin to form hemoglobin tetramer.
  • A classical twin study would be beneficial to investigate the role of genetics and environment in the variation of alpha hemoglobin stabilizing protein expression as this knowledge will enable us to determine further investigations with regards to therapeutic interventions if alpha hemoglobin stabilizing protein is to be a therapeutic agent for β-thalassemia.
  • This study investigates the heritability influence of alpha hemoglobin stabilizing protein expression and factors that may contribute to this.
  • Results indicated that a major proportion of alpha hemoglobin stabilizing protein expression was influenced by genetic heritability (46%) with cis-acting factors accounting for 19% and trans-acting factors at 27%.
  • [MeSH-major] Blood Proteins / genetics. Diseases in Twins / genetics. Gene Expression Regulation. Genetic Predisposition to Disease / genetics. Molecular Chaperones / genetics. beta-Thalassemia / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Microsatellite Repeats / genetics. Middle Aged. RNA, Messenger / genetics. Regulatory Elements, Transcriptional / genetics. Reverse Transcriptase Polymerase Chain Reaction. Twins, Dizygotic / genetics. Twins, Monozygotic / genetics. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21142933.001).
  • [ISSN] 1832-4274
  • [Journal-full-title] Twin research and human genetics : the official journal of the International Society for Twin Studies
  • [ISO-abbreviation] Twin Res Hum Genet
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0000111; United Kingdom / Medical Research Council / / ID51640
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Twin Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AHSP protein, human; 0 / Blood Proteins; 0 / Molecular Chaperones; 0 / RNA, Messenger
  •  go-up   go-down


79. Hu ZW, Luo HB, Xu YM, Guo JW, Deng XL, Tong YW, Tang X: Tumor necrosis factor--alpha gene promoter polymorphisms in Chinese patients with nonalcoholic fatty liver diseases. Acta Gastroenterol Belg; 2009 Apr-Jun;72(2):215-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor necrosis factor--alpha gene promoter polymorphisms in Chinese patients with nonalcoholic fatty liver diseases.
  • BACKGROUND: Nonalcoholic Fatty Liver Disease (NAFLD) encompasses a histopathological spectrum of clinical conditions such as simple fatty liver (steatosis), nonalcoholic steatohepatitis (NASH), and a variant that has degrees of fibrosis.
  • Tumor Necrosis Factor-alpha (TNF-alphalpha) is considered essential for NAFLD.
  • PATIENTS AND METHODS: The TNF-alpha gene polymorphisms at position -238 and -308 were analyzed in 189 Chinese patients with NAFLD and 138 healthy controls by using polymerase chain reaction and restriction fragment length polymorphism assay.
  • The serum levels of TNF-alpha in both patient and control groups were measured by ELISA.
  • The associations of TNF-alpha polymorphism and serum TNF-alpha, and/or insulin resistance, and/or clinical features were analyzed.
  • RESULTS: The carrier frequencies of TNF-alpha gene polymorphism with G/A mutation at -238 were significantly higher in the patients with NAFLD than those in the control subjects (p < 0.05).
  • In addition, the serum level of TNF-alpha was markedly higher in the patients with NAFLD than in the control subjects (p < 0.05).
  • There were significant associations between TNF-alpha gene polymorphism in the -238 A allele and increased serum TNF-alpha, insulin resistance, as well as increased body mass index in the NAFLD patients.
  • CONCLUSIONS: The results indicate that the TNF-alpha gene polymorphism at position -238 is associated with susceptibility of nonalcoholic Fatty Liver Disease in a Chinese population.
  • [MeSH-major] Fatty Liver / genetics. Promoter Regions, Genetic. Tumor Necrosis Factor-alpha / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19637776.001).
  • [ISSN] 1784-3227
  • [Journal-full-title] Acta gastro-enterologica Belgica
  • [ISO-abbreviation] Acta Gastroenterol. Belg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


80. Gu Y, Hu X, Liu C, Qv X, Xu C: Interleukin (IL)-17 promotes macrophages to produce IL-8, IL-6 and tumour necrosis factor-alpha in aplastic anaemia. Br J Haematol; 2008 Jul;142(1):109-14
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin (IL)-17 promotes macrophages to produce IL-8, IL-6 and tumour necrosis factor-alpha in aplastic anaemia.
  • Aplastic anaemia (AA) is thought to be an autoimmune-mediated disease with active destruction of haematopoietic cells through a T helper type 1 (Th1) cell response.
  • It can drive the production of tumour necrosis factor-alpha (TNF-alpha), IL-1 beta, IL-6 and IL-8 by a variety of cells.
  • IL-17 stimulation also resulted in the production of TNF-alpha.
  • These results suggested that elevated expression of IL-17 and IL-17-induced IL-6, IL-8 and TNF-alpha may be involved in the mechanisms of AA.
  • [MeSH-major] Anemia, Aplastic / metabolism. Interleukin-17 / pharmacology. Interleukin-6 / biosynthesis. Interleukin-8 / biosynthesis. Macrophages / metabolism. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Cells, Cultured. Female. Humans. Male. Middle Aged. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation. Young Adult

  • MedlinePlus Health Information. consumer health - Aplastic Anemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18477039.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-17; 0 / Interleukin-6; 0 / Interleukin-8; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


81. Agostoni C, Riva E, Giovannini M, Pinto F, Colombo C, Risé P, Galli C, Marangoni F: Maternal smoking habits are associated with differences in infants' long-chain polyunsaturated fatty acids in whole blood: a case-control study. Arch Dis Child; 2008 May;93(5):414-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Maternal smoking habits are associated with differences in infants' long-chain polyunsaturated fatty acids in whole blood: a case-control study.
  • OBJECTIVE: To study the effects of maternal smoking on the status of long-chain polyunsaturated fatty acids (LCPUFA) in infants' whole-blood lipids.
  • RESULTS: Higher levels of linoleic (LA) and alpha-linolenic acid (ALA) and lower levels of the metabolic products di-homo-gammalinolenic (DHGLA) and arachidonic (AA), of the n-6 series, and docosahexaenoic acid (DHA), of the n-3 series, were found in infants born to late smokers compared with the reference group.

  • MedlinePlus Health Information. consumer health - Smoking.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18426936.001).
  • [ISSN] 1468-2044
  • [Journal-full-title] Archives of disease in childhood
  • [ISO-abbreviation] Arch. Dis. Child.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Fatty Acids, Unsaturated
  •  go-up   go-down


82. Depetris M, Casalis P, Kratje R, Etcheverrigaray M, Oggero M: A scFv antibody fragment as a therapeutic candidate to neutralize a broad diversity of human IFN-alpha subtypes. J Immunol Methods; 2008 May 20;334(1-2):104-13

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A scFv antibody fragment as a therapeutic candidate to neutralize a broad diversity of human IFN-alpha subtypes.
  • In this way, the increased expression of human interferon alpha (hIFN-alpha) is associated with acute viral infections, inflammatory disorders and several autoimmune illnesses, where the cytokine may be a factor in either initiating or maintaining the disease.
  • Currently, there are several mAbs marketed for a variety of indications and many more in clinical trials, in which IFN-alpha represents a potential target for antibody-based therapy.
  • A panel of 11 murine mAbs was prepared using recombinant hIFN-alpha2b as immunogen, all of which bound to the native form of the cytokine with affinity constants ranging from 1.7x10(7) M(-1) to 1.4x10(10) M(-1).
  • Taking into account the characterization of the antibodies and their ability to inhibit the IFN-alpha biological activity, four mAbs were selected to produce scFv fragments.
  • One of these fragments (CA5E6) was able to neutralize a wide spectrum of subtypes of the IFN-alpha family, including the recombinant cytokines hIFN-alpha2a and hIFN-alpha2b and a heterogeneous collection of IFN-alpha produced by activated leukocytes and Namalwa cells.
  • By using this strategy, it was possible to generate a new fragment (EP18) with increased affinity and ability to neutralize a broad diversity of IFN-alpha subtypes.
  • Consequently, the scFv EP18 represents a potential therapeutic agent for those immune and inflammatory diseases which are associated with an increased IFN-alpha expression.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Immunoglobulin Fragments / immunology. Immunoglobulin Variable Region / immunology. Interferon Type I / immunology. Interferon-alpha / immunology
  • [MeSH-minor] Animals. Antibody Affinity. Cloning, Molecular. Epitope Mapping. Female. Humans. Mice. Mice, Inbred BALB C. Neutralization Tests. Polymerase Chain Reaction. Recombinant Proteins

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18394641.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Fragments; 0 / Immunoglobulin Variable Region; 0 / Interferon Type I; 0 / Interferon-alpha; 0 / Recombinant Proteins
  •  go-up   go-down


83. Carturan E, Milanesi O, Kato Y, Giacometti C, Biffanti R, Thiene G, Calabrese F: Viral detection and tumor necrosis factor alpha profile in tracheal aspirates from children with suspicion of myocarditis. Diagn Mol Pathol; 2008 Mar;17(1):21-7
Genetic Alliance. consumer health - Myocarditis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Viral detection and tumor necrosis factor alpha profile in tracheal aspirates from children with suspicion of myocarditis.
  • Pediatric myocarditis is a serious disease resulting in significant morbidity and mortality.
  • Tumor necrosis factor alpha (TNFalpha) is thought to play an important role in the pathogenesis of these disorders.
  • The aim of the present study was to investigate the presence of different viruses and the expression of TNFalpha in children with clinical suspicion of myocarditis.
  • Polymerase chain reaction viral concordance was found in TA and endomyocardial biopsy.
  • [MeSH-major] Myocarditis / diagnosis. Suction. Trachea / metabolism. Trachea / virology. Tumor Necrosis Factor-alpha / analysis
  • [MeSH-minor] Adolescent. Biopsy, Needle. Child. Child, Preschool. DNA, Viral / analysis. Female. Humans. Infant. Infant, Newborn. Male. Polymerase Chain Reaction. RNA, Messenger / analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18303410.001).
  • [ISSN] 1052-9551
  • [Journal-full-title] Diagnostic molecular pathology : the American journal of surgical pathology, part B
  • [ISO-abbreviation] Diagn. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


84. Li Q, Li LY, Mo QH: [A rare thalassemia intermedia case caused by co-existence of Hb H disease (--(SEA)/-alpha(4.2)) and beta-thalassemia major (beta (CD17A)&gt;T/beta (IVS2-654C)&gt;T): implications for prenatal diagnosis]. Nan Fang Yi Ke Da Xue Xue Bao; 2008 Jan;28(1):16-9
MedlinePlus Health Information. consumer health - Prenatal Testing.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A rare thalassemia intermedia case caused by co-existence of Hb H disease (--(SEA)/-alpha(4.2)) and beta-thalassemia major (beta (CD17A)>T/beta (IVS2-654C)>T): implications for prenatal diagnosis].
  • OBJECTIVE: To analyze the relation between the genotype and phenotype in a Chinese patient with thalassemia intermedia and its implications for prenatal diagnosis and genetic counseling of thalassemia intermedia caused by co-existence of Hb H disease and beta; thalassemia major.
  • Genotyping of beta thalassemia mutations and alpha thalassemia deletion were conducted using reverse dot-blot (RDB) assay and gap-PCR, respectively.
  • Prenatal diagnosis for a high-risk fetus in this family was performed by amniotic fluid DNA analysis.
  • RESULTS: The proband was identified as a patient with severe thalassemia intermedia caused by co-existence of Hb H disease (--(SEA)/-alpha (4.2)) and beta-thalassemia major (beta (CD17A)>T/beta (IVS2-654C)>T), whose father was heterozygous for beta thalassemia (beta (CD17A)>T/beta (N)) and alpha-thalassemia trait (--(SEA)/) and the heterozygous for beta thalassemia (beta (IVS2-654C)>T / beta (N)) and silent alpha-thalassemia (-alpha (4.2)/).
  • The result of prenatal diagnosis showed co-existence of beta thalassemia major and silent alpha thalassemia in the high-risk fetus, and the parents requested termination of pregnancy after genetic counseling.
  • CONCLUSION: We report for the first time a rare thalassemia intermedia case resulting from 4 complex alpha/beta thalassemia combination and the molecular pathogenesis of thalassemia intermedia is updated in the Chinese population.
  • The practice of prenatal diagnosis in this case may also provide reference for diagnosis of similar cases.
  • [MeSH-major] Prenatal Diagnosis / methods. alpha-Thalassemia / genetics. beta-Thalassemia / genetics
  • [MeSH-minor] Adult. Child, Preschool. China. Female. Genotype. Humans. Male. Nucleic Acid Hybridization / methods. Phenotype. Polymerase Chain Reaction / methods. Pregnancy

  • Genetic Alliance. consumer health - Thalassemia.
  • Genetic Alliance. consumer health - Beta Thalassemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18227017.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


85. Takenaka A, Kita A, Ikeya M, Arai H, Igarashi K: Galactosamine-induced acute liver injury in rats reduces hepatic alpha-tocopherol transfer protein production. J Nutr Sci Vitaminol (Tokyo); 2007 Aug;53(4):366-71
Hazardous Substances Data Bank. VITAMIN E .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Galactosamine-induced acute liver injury in rats reduces hepatic alpha-tocopherol transfer protein production.
  • The liver plays the main role in the secretion of food-derived alpha-tocopherol into the circulation through the functioning of alpha-tocopherol transfer protein (alpha-TTP).
  • However, the effect of liver disease on alpha-TTP level and alpha-tocopherol metabolism has not been clarified.
  • We examined the amount of liver alpha-TTP and its effect on serum alpha-tocopherol concentration in liver injury.
  • Male Wistar rats were injected intraperitoneally with D-galactosamine at 800 mg/kg body weight, and liver and serum lipid concentrations, alpha-tocopherol concentrations, and hepatic alpha-TTP mRNA and protein levels were measured at 24, 48, and 72 h after injection.
  • The hepatic alpha-TTP mRNA level was reduced throughout the experimental period, and at 48 h after injection the alpha-TTP protein level had begun to decrease.
  • Lipid and alpha-tocopherol concentrations in the serum were decreased at 24 and 48 h after injection and increased at 72 h.
  • Liver lipid concentrations were increased at 24 and 48 h after injection, but the liver alpha-tocopherol concentration was unchanged.
  • These results show that galactosamine-induced liver injury decreases hepatic alpha-TTP synthesis in rats.
  • Serum alpha-tocopherol concentration was not directly affected by the acute change in hepatic alpha-TTP level, suggesting that the chronic changes in alpha-TTP activity would be necessary to regulate serum alpha-tocopherol concentration.
  • [MeSH-major] Carrier Proteins / biosynthesis. Liver Diseases / metabolism
  • [MeSH-minor] Alanine Transaminase / blood. Animals. Aspartate Aminotransferases / blood. Blotting, Western. Cholesterol / blood. Disease Models, Animal. Drug-Induced Liver Injury. Galactosamine. L-Lactate Dehydrogenase / blood. Male. Phospholipids / blood. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Random Allocation. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Triglycerides / blood. alpha-Tocopherol / blood. alpha-Tocopherol / metabolism

  • MedlinePlus Health Information. consumer health - Liver Diseases.
  • Hazardous Substances Data Bank. CHOLESTEROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17934244.001).
  • [ISSN] 0301-4800
  • [Journal-full-title] Journal of nutritional science and vitaminology
  • [ISO-abbreviation] J. Nutr. Sci. Vitaminol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Phospholipids; 0 / RNA, Messenger; 0 / Triglycerides; 0 / alpha-tocopherol transfer protein; 7535-00-4 / Galactosamine; 97C5T2UQ7J / Cholesterol; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase; H4N855PNZ1 / alpha-Tocopherol
  •  go-up   go-down


86. Liu M, Wang X, Yin C, Zhang Z, Lin Q, Zhen Y, Huang H: Targeting TNF-alpha with a tetravalent mini-antibody TNF-TeAb. Biochem J; 2007 Sep 1;406(2):237-46
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting TNF-alpha with a tetravalent mini-antibody TNF-TeAb.
  • Anti-TNF-alpha [anti-(tumour necrosis factor-alpha)] therapy is widely considered to be among the most efficient treatments available for rheumatoid arthritis, psoriatic arthritis and inflammatory bowel disease.
  • In the present study a tetravalent mini-antibody, named 'TNF-TeAb', was constructed by fusing the tetramerization domain of human p53 to the C-terminus of an anti-TNF-scFv [anti-(TNF-alpha-single-chain variable fragment)] via a long and flexible linking peptide derived from human serum albumin.
  • TNF-TeAb was overexpressed as inclusion bodies in the cytoplasm of Escherichia coli, purified to homogeneity by immobilized- metal affinity chromtaography under denaturing conditions and produced in functional form by using an in vitro refolding system.
  • In vitro bioactivity assays suggested that tetramerization of TNF-scFv resulted in an enormous gain in avidity, which endowed TNF-TeAb with a stronger ability to inhibit both receptor binding and cytolytic activity of TNF-alpha.
  • TNF-alpha targeting therapy in rats with collagen-induced arthritis demonstrated that TNF-TeAb provided a much more significant therapeutic effect than did TNF-scFv in suppressing arthritis progression, attenuating inflammation and destruction in joints, and down-regulating pro-inflammatory cytokines and anti-(type II collagen) antibody.
  • The conclusions are therefore (i) that multimerization of the antibody fragment by a self-association peptide is an efficient way to increase its avidity and (ii) that TNF-TeAb has potential applicability for anti-TNF-alpha therapy.
  • [MeSH-major] Antibodies / immunology. Tumor Necrosis Factor-alpha / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cytokine Growth Factor Rev. 2002 Aug-Oct;13(4-5):357-68 [12220549.001]
  • [Cites] J Immunol Methods. 1991 Jun 24;140(1):37-43 [2061612.001]
  • [Cites] Protein Expr Purif. 2002 Nov;26(2):218-28 [12406675.001]
  • [Cites] Arthritis Rheum. 2003 Jan;48(1):35-45 [12528101.001]
  • [Cites] Arthritis Res Ther. 2003;5(3):R122-31 [12723984.001]
  • [Cites] Ann Rheum Dis. 2003 Aug;62(8):707-14 [12860724.001]
  • [Cites] Immunol Cell Biol. 2003 Oct;81(5):354-66 [12969323.001]
  • [Cites] J Biochem. 2004 Apr;135(4):555-65 [15115782.001]
  • [Cites] Cell Immunol. 1993 Jun;149(1):39-49 [8513511.001]
  • [Cites] Cancer Res. 1993 Sep 1;53(17):4026-34 [7689421.001]
  • [Cites] Cancer Res. 1994 Dec 1;54(23):6176-85 [7954464.001]
  • [Cites] J Mol Biol. 1995 Feb 10;246(1):28-34 [7853401.001]
  • [Cites] Science. 1995 Mar 10;267(5203):1498-502 [7878469.001]
  • [Cites] Cell Biophys. 1994;24-25:267-78 [7736532.001]
  • [Cites] Science. 1995 Oct 13;270(5234):286-90 [7569976.001]
  • [Cites] Cancer Res. 1996 Feb 15;56(4):809-15 [8631018.001]
  • [Cites] Cancer Res. 1996 Jul 1;56(13):3055-61 [8674062.001]
  • [Cites] J Immunol. 1996 Oct 1;157(7):2989-97 [8816407.001]
  • [Cites] J R Coll Physicians Lond. 1996 Jul-Aug;30(4):344-51 [8875381.001]
  • [Cites] Br J Cancer. 1996 Nov;74(9):1397-405 [8912535.001]
  • [Cites] Clin Exp Immunol. 1997 Mar;107(3):507-12 [9067525.001]
  • [Cites] Immunotechnology. 1997 Jun;3(2):83-105 [9237094.001]
  • [Cites] Eur J Nucl Med. 1998 Feb;25(2):201-12 [9473271.001]
  • [Cites] N Engl J Med. 2000 Nov 30;343(22):1594-602 [11096166.001]
  • [Cites] J Immunol. 2000 Dec 15;165(12):7240-5 [11120857.001]
  • [Cites] J Biol Chem. 2001 Apr 27;276(17):14385-92 [11278961.001]
  • [Cites] J Leukoc Biol. 1998 Mar;63(3):359-63 [9500524.001]
  • [Cites] Br J Cancer. 1998 May;77(9):1405-12 [9652755.001]
  • [Cites] Cancer Res. 1999 Jan 15;59(2):347-52 [9927045.001]
  • [Cites] Arthritis Rheum. 1999 Jun;42(6):1109-18 [10366103.001]
  • [Cites] Protein Eng. 1999 Jun;12(6):439-46 [10388840.001]
  • [Cites] J Immunol. 1999 Aug 1;163(3):1521-8 [10415055.001]
  • [Cites] Eur J Immunol. 1999 Jul;29(7):2205-12 [10427983.001]
  • [Cites] Curr Opin Immunol. 1999 Oct;11(5):548-57 [10508712.001]
  • [Cites] Biotechnol Appl Biochem. 2006 Mar;43(Pt 3):137-45 [16293104.001]
  • [Cites] J Biol Chem. 2006 Nov 17;281(46):35186-201 [16963450.001]
  • [Cites] Biochemistry. 1992 Feb 18;31(6):1579-84 [1737014.001]
  • [Cites] J Mol Biol. 2000 Jan 21;295(3):627-39 [10623552.001]
  • [Cites] J Biochem. 2004 Jul;136(1):19-28 [15269236.001]
  • [Cites] Proc Natl Acad Sci U S A. 1975 Sep;72(9):3666-70 [1103152.001]
  • [Cites] Nature. 1980 Feb 14;283(5748):666-8 [6153460.001]
  • [Cites] Arthritis Rheum. 1981 Jun;24(6):781-9 [6972765.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Jan;79(1):71-5 [6275391.001]
  • [Cites] J Exp Med. 1986 Jun 1;163(6):1433-50 [3486936.001]
  • [Cites] FASEB J. 1988 Nov;2(14):2950-6 [3053308.001]
  • [Cites] J Immunol. 1989 Jun 1;142(11):3884-93 [2469726.001]
  • [Cites] J Immunol. 1990 Dec 15;145(12):4181-4 [2147937.001]
  • [Cites] Arthritis Res. 2002;4(5):R7 [12223110.001]
  • (PMID = 17472572.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 9007-34-5 / Collagen
  • [Other-IDs] NLM/ PMC1948971
  •  go-up   go-down


87. Guiyedi V, Chanseaud Y, Fesel C, Snounou G, Rousselle JC, Lim P, Koko J, Namane A, Cazenave PA, Kombila M, Pied S: Self-reactivities to the non-erythroid alpha spectrin correlate with cerebral malaria in Gabonese children. PLoS One; 2007;2(4):e389
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Self-reactivities to the non-erythroid alpha spectrin correlate with cerebral malaria in Gabonese children.
  • Some of the antibodies produced recognize self-components and are correlated with disease severity in P. falciparum malaria.
  • We show here a correlation between self-antibody responses to a human brain protein and high levels of circulating TNF alpha (TNFalpha), with the manifestation of CM in Gabonese children.
  • We found that 90% of CM patients displayed reactivity to a high-molecular mass band containing the spectrin non-erythroid alpha chain.
  • [MeSH-minor] Child. Cohort Studies. Gabon. Humans. Immunoglobulin G / immunology. Mass Spectrometry. Multivariate Analysis. Tumor Necrosis Factor-alpha / metabolism

  • Genetic Alliance. consumer health - Malaria.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Trends Neurosci. 2000 Jan;23(1):20-6 [10631785.001]
  • [Cites] J Neurosci Res. 2005 Jul 1;81(1):53-61 [15952172.001]
  • [Cites] Infect Immun. 2000 Mar;68(3):1183-8 [10678924.001]
  • [Cites] Eur Cytokine Netw. 2000 Mar;11(1):113-8 [10705308.001]
  • [Cites] Mem Inst Oswaldo Cruz. 2000 Mar-Apr;95(2):199-207 [10733739.001]
  • [Cites] J Med Microbiol. 2000 Apr;49(4):305-11 [10755623.001]
  • [Cites] Am J Trop Med Hyg. 2001 Jan-Feb;64(1-2 Suppl):iv-vii [11425185.001]
  • [Cites] Physiol Rev. 2001 Jul;81(3):1353-92 [11427698.001]
  • [Cites] Ann Med Interne (Paris). 1998 Feb;149(1):30-3 [11490514.001]
  • [Cites] Nature. 2002 Feb 7;415(6872):673-9 [11832955.001]
  • [Cites] Clin Exp Immunol. 2002 Jan;127(1):158-64 [11882047.001]
  • [Cites] Arthritis Rheum. 2002 Dec;46(12):3290-300 [12483734.001]
  • [Cites] J Infect Dis. 2003 Feb 1;187(3):522-5 [12552440.001]
  • [Cites] J Neuroimmunol. 2003 May;138(1-2):156-61 [12742665.001]
  • [Cites] Mol Cell Biol. 2003 Jul;23(13):4449-60 [12808088.001]
  • [Cites] Neurobiol Dis. 2003 Jul;13(2):75-88 [12828932.001]
  • [Cites] Neurosci Res. 2003 Dec;47(4):373-82 [14630341.001]
  • [Cites] Eur Cytokine Netw. 2003 Oct-Dec;14(4):238-41 [14715416.001]
  • [Cites] Arthritis Rheum. 2004 Apr;50(4):1239-47 [15077307.001]
  • [Cites] J Neuroimmunol. 2004 Jul;152(1-2):83-97 [15223241.001]
  • [Cites] Dermatol Online J. 2004;10(1):7 [15347489.001]
  • [Cites] Lancet. 1968 Jun 22;1(7556):1342-6 [4172652.001]
  • [Cites] Clin Exp Immunol. 1978 Apr;32(1):41-5 [352584.001]
  • [Cites] J Neuroimmunol. 1981 Mar;1(1):27-39 [6173395.001]
  • [Cites] Clin Exp Immunol. 1982 Aug;49(2):310-6 [6982135.001]
  • [Cites] Trans R Soc Trop Med Hyg. 1983;77(2):185-8 [6346590.001]
  • [Cites] Eur J Immunol. 1984 May;14(5):435-41 [6609826.001]
  • [Cites] N Engl J Med. 1989 Jun 15;320(24):1586-91 [2657427.001]
  • [Cites] Immunol Today. 1991 Apr;12(4):105-10 [2059311.001]
  • [Cites] J Clin Lab Immunol. 1991 Jul;35(3):109-12 [1668763.001]
  • [Cites] Immunol Today. 1992 Dec;13(12):490-4 [1463581.001]
  • [Cites] Immunology. 1993 Aug;79(4):653-7 [8406592.001]
  • [Cites] Eur J Immunol. 1993 Nov;23(11):2851-9 [8223861.001]
  • [Cites] Lancet. 1993 Nov 27;342(8883):1333-4 [7901638.001]
  • [Cites] Scand J Immunol. 1994 Jan;39(1):79-87 [8290896.001]
  • [Cites] Clin Exp Immunol. 1994 Feb;95(2):304-9 [8306506.001]
  • [Cites] S Afr Med J. 1993 Sep;83(9):660-2 [8310360.001]
  • [Cites] QJM. 1994 Sep;87(9):523-8 [7953500.001]
  • [Cites] Eur J Immunol. 1995 May;25(5):1358-65 [7774639.001]
  • [Cites] Eur J Immunol. 1995 Sep;25(9):2598-604 [7589132.001]
  • [Cites] Scand J Immunol. 1996 Mar;43(3):263-70 [8602459.001]
  • [Cites] Scand J Immunol. 1996 Sep;44(3):243-51 [8795718.001]
  • [Cites] Clin Immunol Immunopathol. 1996 Sep;80(3 Pt 1):311-20 [8811053.001]
  • [Cites] Pediatr Neurol. 1996 Jul;15(1):41-9 [8858700.001]
  • [Cites] Biochem J. 1996 Nov 1;319 ( Pt 3):683-90 [8920967.001]
  • [Cites] Science. 1997 Apr 25;276(5312):604-7 [9110981.001]
  • [Cites] J Neurosci. 2005 Aug 10;25(32):7352-8 [16093385.001]
  • [Cites] Lancet Neurol. 2005 Dec;4(12):827-40 [16297841.001]
  • [Cites] Neurology. 2005 Dec 13;65(11):1730-6 [16344514.001]
  • [Cites] Neurochem Int. 2006 Jan;48(2):108-13 [16236382.001]
  • [Cites] Acta Neurochir (Wien). 2006 Feb;148(2):199-205; discussion 205 [16362182.001]
  • [Cites] J Neuroimmunol. 2006 Apr;173(1-2):96-107 [16414123.001]
  • [Cites] Arthritis Res Ther. 2006;8(2):R38 [16469116.001]
  • [Cites] Physiol Res. 1999;48(5):383-7 [10625228.001]
  • [Cites] Lupus. 2006;15(7):428-30 [16898177.001]
  • [Cites] J Neuroimmunol. 2006 Oct;179(1-2):53-64 [16893572.001]
  • [Cites] J Infect. 2007 Jan;54(1):e1-3 [16647756.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Dec 26;103(52):19854-9 [17170137.001]
  • [Cites] J Infect Dis. 2007 Apr 1;195(7):921-3 [17330779.001]
  • [Cites] Neuron. 1998 Jan;20(1):153-63 [9459451.001]
  • [Cites] J Clin Immunol. 1999 Mar;19(2):109-15 [10226885.001]
  • [Cites] J Infect Dis. 2005 Jan 1;191(1):117-21 [15593012.001]
  • [Cites] Immunogenetics. 2005 May;57(3-4):293-6 [15900502.001]
  • [Cites] Parasitology. 1999 Dec;119 ( Pt 6):543-53 [10633915.001]
  • (PMID = 17460756.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin G; 0 / Tumor Necrosis Factor-alpha; 12634-43-4 / Spectrin
  • [Other-IDs] NLM/ PMC1851099
  • [General-notes] NLM/ Original DateCompleted: 20070803
  •  go-up   go-down


88. Fiaccavento R, Carotenuto F, Minieri M, Masuelli L, Vecchini A, Bei R, Modesti A, Binaglia L, Fusco A, Bertoli A, Forte G, Carosella L, Di Nardo P: Alpha-linolenic acid-enriched diet prevents myocardial damage and expands longevity in cardiomyopathic hamsters. Am J Pathol; 2006 Dec;169(6):1913-24
MedlinePlus Health Information. consumer health - Cardiomyopathy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha-linolenic acid-enriched diet prevents myocardial damage and expands longevity in cardiomyopathic hamsters.
  • Randomized clinical trials have demonstrated that the increased intake of omega-3 polyunsaturated fatty acids significantly reduces the risk of ischemic cardiovascular disease, but no investigations have been performed in hereditary cardiomyopathies with diffusely damaged myocardium.
  • In the present study, delta-sarcoglycan-null cardiomyopathic hamsters were fed from weaning to death with an alpha-linolenic acid (ALA)-enriched versus standard diet.
  • In fact, ALA administration preserved plasmalemma and mitochondrial membrane integrity, thus maintaining proper cell/extracellular matrix contacts and signaling, as well as a normal gene expression profile (myosin heavy chain isoforms, atrial natriuretic peptide, transforming growth factor-beta1) and a limited extension of fibrotic areas within ALA-fed cardiomyopathic hearts.
  • [MeSH-major] Cardiomegaly / diet therapy. Cardiomyopathies / diet therapy. Dietary Fats, Unsaturated / therapeutic use. Fatty Acids, Omega-3 / therapeutic use. alpha-Linolenic Acid / therapeutic use
  • [MeSH-minor] Animals. Cricetinae. Disease Models, Animal. Endomyocardial Fibrosis / pathology. Endomyocardial Fibrosis / prevention & control. Fatty Acids / blood. Longevity. Myocardial Contraction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem Soc Trans. 2005 Dec;33(Pt 6):1254-5 [16246091.001]
  • [Cites] Curr Opin Cell Biol. 2005 Apr;17(2):174-82 [15780594.001]
  • [Cites] Curr Atheroscler Rep. 2005 Nov;7(6):435-45 [16256001.001]
  • [Cites] FASEB J. 2005 Nov;19(13):1863-5 [16150801.001]
  • [Cites] Circulation. 2005 Nov 22;112(21):3232-8 [16301356.001]
  • [Cites] Am J Cardiol. 2005 Dec 1;96(11):1521-9 [16310434.001]
  • [Cites] Nat Immunol. 2005 Dec;6(12):1191-7 [16369558.001]
  • [Cites] J Membr Biol. 2005 Jul;206(2):85-102 [16456720.001]
  • [Cites] J Clin Invest. 2006 Mar;116(3):598-606 [16511592.001]
  • [Cites] Circulation. 1992 May;85(5):1734-42 [1533350.001]
  • [Cites] Int J Cancer. 1993 Apr 1;53(6):988-93 [8473057.001]
  • [Cites] J Clin Invest. 1993 Jun;91(6):2861-5 [8514894.001]
  • [Cites] Prostaglandins Leukot Essent Fatty Acids. 1995 Feb-Mar;52(2-3):199-203 [7784458.001]
  • [Cites] Hum Mol Genet. 1997 Apr;6(4):601-7 [9097966.001]
  • [Cites] Lab Invest. 1997 Nov;77(5):489-502 [9389792.001]
  • [Cites] Am J Pathol. 1998 Nov;153(5):1623-30 [9811355.001]
  • [Cites] Prev Med. 1999 May;28(5):520-9 [10329343.001]
  • [Cites] J Biol Chem. 1957 May;226(1):497-509 [13428781.001]
  • [Cites] J Nutr. 2004 Dec;134(12):3250-6 [15570021.001]
  • [Cites] J Clin Invest. 2004 Dec;114(11):1577-85 [15578090.001]
  • [Cites] Nutr Rev. 2004 Nov;62(11):414-26 [15622714.001]
  • [Cites] Am J Clin Nutr. 2000 Jan;71(1 Suppl):343S-8S [10617994.001]
  • [Cites] Cardiovasc Drugs Ther. 1999 Nov;13(6):525-30 [10686662.001]
  • [Cites] J Cell Sci. 2000 Jul;113 ( Pt 14):2535-44 [10862711.001]
  • [Cites] Circulation. 2000 Jul 11;102(2):246-52 [10889138.001]
  • [Cites] J Biol Chem. 2000 Jul 21;275(29):22293-9 [10801788.001]
  • [Cites] J Exp Med. 2000 Oct 16;192(8):1197-204 [11034610.001]
  • [Cites] J Lipid Res. 2001 Jan;42(1):96-105 [11160370.001]
  • [Cites] Trends Cardiovasc Med. 2000 Aug;10(6):238-45 [11282301.001]
  • [Cites] Circulation. 2002 Jan 29;105(4):502-8 [11815435.001]
  • [Cites] Ann Pharmacother. 2002 May;36(5):751-7 [11978147.001]
  • [Cites] Circulation. 2002 May 14;105(19):2303-8 [12010914.001]
  • [Cites] Life Sci. 2002 Oct 4;71(20):2369-81 [12231398.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1226-31 [12552126.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):1751-6 [12578976.001]
  • [Cites] Mol Cell Biochem. 2003 Oct;252(1-2):73-81 [14577578.001]
  • [Cites] Cardiovasc Res. 2003 Nov 1;60(2):376-87 [14613867.001]
  • [Cites] Circ Res. 2004 Apr 30;94(8):1023-31 [15117830.001]
  • [Cites] FASEB J. 2004 Jun;18(9):1040-2 [15084525.001]
  • [Cites] Clin Sci (Lond). 2004 Jul;107(1):1-11 [15132735.001]
  • [Cites] Eur J Heart Fail. 2004 Aug;6(5):635-41 [15302013.001]
  • [Cites] Prev Cardiol. 2003 Summer;6(3):136-46 [15319583.001]
  • [Cites] Nutr Metab Cardiovasc Dis. 2004 Jun;14(3):162-9 [15330276.001]
  • [Cites] Lipids. 2004 Apr;39(4):325-34 [15357020.001]
  • [Cites] Prog Lipid Res. 2004 Sep;43(5):383-402 [15458813.001]
  • [Cites] N Engl J Med. 1988 Mar 3;318(9):549-57 [3277056.001]
  • [Cites] J Physiol. 1991 Jun;437:655-72 [1890654.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2005 May;288(5):H2131-9 [15840903.001]
  • [Cites] BMJ. 2005 Apr 30;330(7498):991 [15820966.001]
  • [Cites] Exp Gerontol. 2005 May;40(5):369-76 [15919588.001]
  • [Cites] JAMA. 2005 Jun 15;293(23):2884-91 [15956633.001]
  • [Cites] Biochemistry. 2005 Aug 2;44(30):10164-9 [16042393.001]
  • [Cites] Muscle Nerve. 2005 Nov;32(5):563-76 [15937871.001]
  • [Cites] J Mol Cell Cardiol. 2005 Jan;38(1):81-91 [15623424.001]
  • [Cites] J Pathol. 2005 Feb;205(3):397-407 [15682436.001]
  • [Cites] Lipids. 2004 Oct;39(10):955-61 [15691017.001]
  • [Cites] Circulation. 2005 Oct 25;112(17):2650-9 [16230483.001]
  • (PMID = 17148657.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Fats, Unsaturated; 0 / Fatty Acids; 0 / Fatty Acids, Omega-3; 0RBV727H71 / alpha-Linolenic Acid
  • [Other-IDs] NLM/ PMC1762468
  •  go-up   go-down


89. Bruun JM, Roeske-Nielsen A, Richelsen B, Fredman P, Buschard K: Sulfatide increases adiponectin and decreases TNF-alpha, IL-6, and IL-8 in human adipose tissue in vitro. Mol Cell Endocrinol; 2007 Jan 15;263(1-2):142-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sulfatide increases adiponectin and decreases TNF-alpha, IL-6, and IL-8 in human adipose tissue in vitro.
  • Type 2 diabetes is associated with decreased levels of the glycosphingolipid sulfatide, as well as a state of low-grade inflammation.
  • In the present study, the effects of sulfatide on adipokine (adiponectin, TNF-alpha, IL-6, and IL-8) production in human adipose tissue (AT) was investigated in vitro.
  • Only the C16:0 isoform decreased TNF-alpha, IL-6, and IL-8 production 20-30%.
  • The C16:0 sulfatide has been shown to activate potassium channels in beta-cells, and glibenclamide, an ATP-sensitive K+-(KATP) channel blocker, reversed the C16:0-induced decrement in stimulated TNF-alpha, IL-6, and IL-8 release in adipocytes.
  • Glibenclamide on its own was without effect on the production of adiponectin, TNF-alpha, IL-6, and IL-8.
  • Accordingly, the reported low serum levels of sulfatide in patients with type 2 diabetes might be of importance in relation to the chronic low-grade inflammatory state found in this disease.
  • [MeSH-major] Adiponectin / metabolism. Adipose Tissue / drug effects. Interleukin-6 / metabolism. Interleukin-8 / metabolism. Sulfoglycosphingolipids / pharmacology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Adipocytes / cytology. Adipocytes / metabolism. Adult. Animals. Cells, Cultured. Humans. Obesity / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Swine. Women

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17097222.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Interleukin-6; 0 / Interleukin-8; 0 / RNA, Messenger; 0 / Sulfoglycosphingolipids; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


90. Ghebranious N, Mallum J: A Single multiplexed allele-specific polymerase chain reaction for simultaneous detection of alpha1-antitrypsin S and Z mutations. Genet Test; 2005;9(3):185-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A Single multiplexed allele-specific polymerase chain reaction for simultaneous detection of alpha1-antitrypsin S and Z mutations.
  • Alpha1-antitrypsin (AAT) deficiency is an inherited disorder that can cause lung disease in adults and liver disease in adults and children.
  • We have developed a simple multiplexed allele-specific-PCR to detect both the S and Z mutations and the corresponding wild-type alleles.
  • Polymerase chain reaction (PCR) product could be resolved on an agarose gel or using any fluorescent gel detection system.
  • We obtained accurate genotyping results for the four alleles; the S, Z, and their corresponding wild-type alleles for all investigated samples simultaneously.
  • [MeSH-major] Alleles. Mutation. Polymerase Chain Reaction / methods. alpha 1-Antitrypsin / genetics

  • Coriell Cell Repositories. culture/stock collections - Coriell Cell Repositories .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16225408.001).
  • [ISSN] 1090-6576
  • [Journal-full-title] Genetic testing
  • [ISO-abbreviation] Genet. Test.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / alpha 1-Antitrypsin
  •  go-up   go-down


91. Kassi E, Vlachoyiannopoulos PG, Kominakis A, Kiaris H, Moutsopoulos HM, Moutsatsou P: Estrogen receptor alpha gene polymorphism and systemic lupus erythematosus: a possible risk? Lupus; 2005;14(5):391-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Estrogen receptor alpha gene polymorphism and systemic lupus erythematosus: a possible risk?
  • Genetic alterations in the exon 8-coding region of the estrogen receptor alpha alter the intracellular signalling of estrogens, leading in enhanced or diminished activity.
  • We investigated whether genetic alterations in exon 8 of ERalpha gene are associated with the occurrence and clinical features of lupus disease.
  • The coding region of ERalpha exon 8 was subjected to mutation analysis using the polymerase chain reaction, denaturing gradient gel electrophoresis and sequence analysis, using DNA isolated from whole blood of 36 female patients and 38 healthy females.
  • Clinical and laboratory parameters were available from the patients' files.
  • We identified the codon 594 polymorphism either in homozygous for the wild type gene (ACG/ACG) or heterozygous (ACG/ACA), both in patients and healthy females.
  • Odds ratio estimate revealed that carriers of ACG/ACA genotype have three-fold higher risk of developing lupus disease (OR = 3.129, 95% CI 1.181-8.292).
  • The heterozygous patients were associated significantly with an early age at disease onset (ANOVA test, P < 0.05).
  • We conclude that estrogen receptor alpha codon 594 genotype may influence the development of systemic lupus erythematosus at a younger age, as well as a certain disease clinical pattern.
  • [MeSH-major] Estrogen Receptor alpha / genetics. Genetic Predisposition to Disease. Lupus Erythematosus, Systemic / genetics. Polymorphism, Genetic
  • [MeSH-minor] Adult. Alleles. DNA Mutational Analysis. Electrophoresis, Polyacrylamide Gel. Female. Gene Frequency. Genotype. Humans. Middle Aged. Odds Ratio. Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Lupus.
  • Genetic Alliance. consumer health - Systemic lupus erythematosus.
  • MedlinePlus Health Information. consumer health - Lupus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15934440.001).
  • [ISSN] 0961-2033
  • [Journal-full-title] Lupus
  • [ISO-abbreviation] Lupus
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha
  •  go-up   go-down


92. Gillmore JD, Lachmann HJ, Rowczenio D, Gilbertson JA, Zeng CH, Liu ZH, Li LS, Wechalekar A, Hawkins PN: Diagnosis, pathogenesis, treatment, and prognosis of hereditary fibrinogen A alpha-chain amyloidosis. J Am Soc Nephrol; 2009 Feb;20(2):444-51
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis, pathogenesis, treatment, and prognosis of hereditary fibrinogen A alpha-chain amyloidosis.
  • Mutations in the fibrinogen A alpha-chain gene are the most common cause of hereditary renal amyloidosis in the United Kingdom.
  • Previous reports of fibrinogen A alpha-chain amyloidosis have been in isolated kindreds, usually in the context of a novel amyloidogenic mutation.
  • Median age at presentation was 58 yr, and renal involvement led to diagnosis in all cases.
  • Even after a median follow-up of 4 yr, clinically significant extra-renal disease was rare.
  • A family history of renal disease was frequently absent.
  • In summary, fibrinogen amyloidosis is predominantly a renal disease characterized by variable penetrance, distinctive histological appearance, proteinuria, and progressive renal impairment.
  • Survival is markedly better than observed with systemic AL amyloidosis, and outcomes with renal replacement therapy are comparable to those for age-matched individuals with nondiabetic renal disease.
  • [MeSH-major] Amyloidosis / diagnosis. Amyloidosis / mortality. Amyloidosis / physiopathology. Fibrinogen / chemistry

  • Genetic Alliance. consumer health - Amyloidosis.
  • MedlinePlus Health Information. consumer health - Amyloidosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Pathol. 1999 Sep;155(3):695-702 [10487826.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Apr 13;257(2):584-8 [10198255.001]
  • [Cites] Kidney Int. 2005 Nov;68(5):1994-8 [16221199.001]
  • [Cites] Am J Transplant. 2006 Oct;6(10):2342-7 [16925563.001]
  • [Cites] Blood. 2007 Mar 1;109(5):1971-4 [17082318.001]
  • [Cites] N Engl J Med. 2007 Jun 7;356(23):2361-71 [17554117.001]
  • [Cites] Br J Haematol. 2008 Feb;140(4):365-77 [18162121.001]
  • [Cites] QJM. 2000 May;93(5):269-75 [10825402.001]
  • [Cites] Am J Pathol. 2000 Jun;156(6):1911-7 [10854214.001]
  • [Cites] Genomics. 2001 Mar 15;72(3):272-7 [11401442.001]
  • [Cites] Kidney Int. 2002 Jan;61(1):1-9 [11786079.001]
  • [Cites] Ann Intern Med. 2004 Jan 20;140(2):85-93 [14734330.001]
  • [Cites] Gastroenterology. 2004 May;126(5):1416-22 [15131802.001]
  • [Cites] N Engl J Med. 1990 Aug 23;323(8):508-13 [2377176.001]
  • [Cites] Atherosclerosis. 1991 Aug;89(2-3):137-41 [1793440.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Aug 15;89(16):7389-93 [1502149.001]
  • [Cites] Int J Artif Organs. 1993 Jan;16(1):31-6 [8458668.001]
  • [Cites] Nature. 1993 Apr 8;362(6420):553-7 [8464497.001]
  • [Cites] Nat Genet. 1993 Mar;3(3):252-5 [8097946.001]
  • [Cites] J Clin Invest. 1994 Feb;93(2):731-6 [8113408.001]
  • [Cites] QJM. 1995 Oct;88(10):695-702 [7493166.001]
  • [Cites] Blood. 1996 May 15;87(10):4197-203 [8639778.001]
  • [Cites] J Clin Invest. 1996 Jun 15;97(12):2714-21 [8675681.001]
  • [Cites] N Engl J Med. 1997 Apr 24;336(17):1202-7 [9110907.001]
  • [Cites] Blood. 1997 Dec 15;90(12):4799-805 [9389696.001]
  • [Cites] Kidney Int. 1998 Feb;53(2):276-81 [9461086.001]
  • [Cites] Nephrol Dial Transplant. 1998 Aug;13(8):2004-12 [9719155.001]
  • [Cites] Am J Pathol. 1999 Jan;154(1):221-7 [9916936.001]
  • [Cites] Am J Kidney Dis. 2004 Dec;44(6):1103-9 [15558533.001]
  • (PMID = 19073821.001).
  • [ISSN] 1533-3450
  • [Journal-full-title] Journal of the American Society of Nephrology : JASN
  • [ISO-abbreviation] J. Am. Soc. Nephrol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G7900510
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid; 9001-32-5 / Fibrinogen
  • [Other-IDs] NLM/ PMC2637055
  •  go-up   go-down


93. Beyer K, Domingo-Sàbat M, Humbert J, Carrato C, Ferrer I, Ariza A: Differential expression of alpha-synuclein, parkin, and synphilin-1 isoforms in Lewy body disease. Neurogenetics; 2008 Jul;9(3):163-72
MedlinePlus Health Information. consumer health - Lewy Body Disease.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression of alpha-synuclein, parkin, and synphilin-1 isoforms in Lewy body disease.
  • Alpha-synuclein, parkin, and synphilin-1 are proteins mainly involved in the pathogenesis of Lewy body (LB) diseases. mRNAs of all three undergo alternative splicing, so that the existence of various isoforms has been described.
  • Since increasing evidence supports the importance of differential isoform-expression changes in disease development, we have established isoform-expression profiles in frontal cortices of LB disease brains in comparison with those of Alzheimer disease (AD) and control frontal cortices.
  • The differential expression of four alpha-synuclein, seven parkin, and four synphilin-1 isoforms was ascertained by the use of isoform-specific primers and relative expression analysis with SybrGreen and beta-actin as an internal standard.
  • The establishment of isoform-expression profiles revealed that these are disease specific.
  • Moreover, isoform-expression deregulation of mainly one gene in each disease could be observed.
  • All four alpha-synuclein isoforms were affected in the case of the pure form of dementia with LB, most parkin transcript variants in common LB disease, and all synphilin-1 isoforms in Parkinson disease.
  • Finally, the existence of a proprietary isoform-expression profile in common LB disease indicates that this disease develops as a result of its own molecular mechanisms, and so, at the molecular level, it does not exactly share changes found in pure dementia with LB and AD.
  • In conclusion, isoform-expression profiles in LB diseases represent additional evidence for the direct involvement of isoform-expression deregulation in the development of neurodegenerative disorders.
  • [MeSH-major] Carrier Proteins / genetics. Lewy Body Disease / genetics. Nerve Tissue Proteins / genetics. Ubiquitin-Protein Ligases / genetics. alpha-Synuclein / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. Alzheimer Disease / genetics. Alzheimer Disease / metabolism. Base Sequence. Case-Control Studies. DNA Primers / genetics. Female. Frontal Lobe / metabolism. Gene Expression. Gene Expression Profiling. Humans. Male. Middle Aged. Multiple System Atrophy / genetics. Multiple System Atrophy / metabolism. Parkinson Disease / genetics. Parkinson Disease / metabolism. Polymerase Chain Reaction. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18335262.001).
  • [ISSN] 1364-6753
  • [Journal-full-title] Neurogenetics
  • [ISO-abbreviation] Neurogenetics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA Primers; 0 / Nerve Tissue Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / SNCAIP protein, human; 0 / alpha-Synuclein; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / parkin protein
  •  go-up   go-down


94. Gispert S, Trenkwalder C, Mota-Vieira L, Kostic V, Auburger G: Failure to find alpha-synuclein gene dosage changes in 190 patients with familial Parkinson disease. Arch Neurol; 2005 Jan;62(1):96-8
MedlinePlus Health Information. consumer health - Parkinson's Disease.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Failure to find alpha-synuclein gene dosage changes in 190 patients with familial Parkinson disease.
  • BACKGROUND: Recently, a triplication of the alpha-synuclein locus was found associated with autosomal dominant Parkinson disease in a large family.
  • OBJECTIVE: To determine whether a triplication or some other dosage alteration in the alpha-synuclein gene is present in one or more patients with familial PD in a large multinational collective.
  • MAIN OUTCOME MEASURES: Alpha-synuclein gene dosage values measured with real-time polymerase chain reaction.
  • RESULTS: None of the samples showed alpha-synuclein triplication, duplication, or deletion.
  • CONCLUSION: Alterations in alpha-synuclein gene dosage are rare in familial PD.
  • [MeSH-major] Family Health. Gene Dosage. Nerve Tissue Proteins / genetics. Parkinson Disease / genetics
  • [MeSH-minor] Adult. Aged. Exons. Female. Humans. Male. Middle Aged. RNA, Messenger / biosynthesis. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction / methods. Synucleins. alpha-Synuclein

  • Genetic Alliance. consumer health - Parkinson Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15642855.001).
  • [ISSN] 0003-9942
  • [Journal-full-title] Archives of neurology
  • [ISO-abbreviation] Arch. Neurol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / SNCA protein, human; 0 / Synucleins; 0 / alpha-Synuclein
  •  go-up   go-down


95. Ko CW, Cuthbert RJ, Orsi NM, Brooke DA, Perry SL, Markham AF, Coletta PL, Hull MA: Lack of interleukin-4 receptor alpha chain-dependent signalling promotes azoxymethane-induced colorectal aberrant crypt focus formation in Balb/c mice. J Pathol; 2008 Apr;214(5):603-9
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of interleukin-4 receptor alpha chain-dependent signalling promotes azoxymethane-induced colorectal aberrant crypt focus formation in Balb/c mice.
  • Interleukin (IL)-4 receptor (IL-4R) alpha chain-dependent signalling by IL-4 and IL-13 promotes tumour growth and metastasis in mouse models of colorectal cancer.
  • However, the role of IL-4R alpha-dependent signalling during the early, pre-malignant stages of colorectal carcinogenesis has not been investigated.
  • Therefore, we investigated the effect of deletion of the IL-4R alpha gene on azoxymethane-induced colorectal aberrant crypt focus (ACF) multiplicity and size in Balb/c mice.
  • IL-4R alpha(-/-) mice developed significantly more ACFs [median 8, inter-quartile range (IQR) 4-11.5; n = 9] than wild-type (WT) animals (median 4, IQR 1-6; n = 9; p = 0.04, Mann-Whitney U-test).
  • There were significantly higher levels of IL-4 in serum from azoxymethane- and sham-treated IL-4R alpha(-/-) mice than WT animals, but no difference in serum IL-13 levels.
  • In the absence of functional IL-4Rs, IL-13 can also signal via the IL-13R alpha2 receptor, leading to induction of transforming growth factor (TGF) beta, which has pro-tumourigenic activity at early stages of intestinal tumourigenesis.
  • We found that mucosal TGFbeta mRNA levels and intestinal epithelial cell TGFbeta immunoreactivity were significantly higher in IL-4R alpha(-/-) mice than in WT animals.
  • In summary, IL-4R alpha-dependent signalling has a protective, anti-neoplastic role during the post-initiation phase of azoxymethane-induced colorectal carcinogenesis in Balb/c mice.
  • Our data should prompt thorough investigation of the role of IL-4R alpha-dependent signalling during human colorectal carcinogenesis, particularly as antagonism of IL-4R signalling represents a therapeutic strategy for asthma and other allergic diseases.

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2008 Pathological Society of Great Britain and Ireland
  • (PMID = 18220315.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] ENG
  • [Grant] United Kingdom / Medical Research Council / / G116/146; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Il4ra protein, mouse; 0 / Interleukin-13; 0 / Receptors, Cell Surface; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; MO0N1J0SEN / Azoxymethane
  •  go-up   go-down


96. Badoual C, Bouchaud G, Agueznay Nel H, Mortier E, Hans S, Gey A, Fernani F, Peyrard S, -Puig PL, Bruneval P, Sastre X, Plet A, Garrigue-Antar L, Quintin-Colonna F, Fridman WH, Brasnu D, Jacques Y, Tartour E: The soluble alpha chain of interleukin-15 receptor: a proinflammatory molecule associated with tumor progression in head and neck cancer. Cancer Res; 2008 May 15;68(10):3907-14
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The soluble alpha chain of interleukin-15 receptor: a proinflammatory molecule associated with tumor progression in head and neck cancer.
  • Interleukin (IL)-15 is a proinflammatory cytokine, as it induces the production of inflammatory cytokines [IL-6, tumor necrosis factor alpha (TNFalpha), IL-17, etc.].
  • A correlation between high intratumoral IL-15 concentrations and poor clinical outcome in lung and head and neck cancer patients has been recently reported.
  • The purpose of this study was to investigate the role of the soluble alpha chain of IL-15 receptor (sIL-15Ralpha), a natural regulator of IL-15, in head and neck cancer.
  • Increased serum sIL-15Ralpha concentrations were found in head and neck cancer patients and were closely correlated with poor clinical outcome both in terms of locoregional control and survival even on multivariate analysis. sIL-15Ralpha was mainly produced by tumor cells via proteolytic cleavage of IL-15Ralpha mediated by ADAM-17.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Head and Neck Neoplasms / pathology. Interleukin-15 Receptor alpha Subunit / physiology
  • [MeSH-minor] ADAM Proteins / biosynthesis. Cross-Linking Reagents / pharmacology. Disease Progression. Humans. Inflammation. Interleukin-15 / metabolism. Models, Biological. Multivariate Analysis. Prognosis. Protein Isoforms. Radioimmunoassay

  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18483276.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cross-Linking Reagents; 0 / Interleukin-15; 0 / Interleukin-15 Receptor alpha Subunit; 0 / Protein Isoforms; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
  •  go-up   go-down


97. Ellis CE, Murphy EJ, Mitchell DC, Golovko MY, Scaglia F, Barceló-Coblijn GC, Nussbaum RL: Mitochondrial lipid abnormality and electron transport chain impairment in mice lacking alpha-synuclein. Mol Cell Biol; 2005 Nov;25(22):10190-201
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mitochondrial lipid abnormality and electron transport chain impairment in mice lacking alpha-synuclein.
  • The presynaptic protein alpha-synuclein, implicated in Parkinson disease (PD), binds phospholipids and has a role in brain fatty acid (FA) metabolism.
  • In mice lacking alpha-synuclein (Snca-/-), total brain steady-state mass of the mitochondria-specific phospholipid, cardiolipin, is reduced 22% and its acyl side chains show a 51% increase in saturated FAs and a 25% reduction in essential n-6, but not n-3, polyunsaturated FAs.
  • Consistent with these changes, more ordered lipid head group and acyl chain packing with enhanced rotational motion of diphenylhexatriene (DPH) about its long axis were demonstrated in time-resolved DPH fluorescence lifetime experiments.
  • These abnormalities in mitochondrial membrane properties were associated with a 15% reduction in linked complex I/III activity of the electron transport chain, without reductions in mitochondrial number, complex II/III activity, or individual complex I, II, III, or IV activity.
  • Thus, altered membrane composition and structure and impaired complex I/III function in Snca-/- brain suggest a relationship between alpha-synuclein's role in brain lipid metabolism, mitochondrial function, and PD.

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. PALMITIC ACID .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] EMBO J. 2000 Apr 17;19(8):1777-83 [10775262.001]
  • [Cites] J Lipid Res. 2000 May;41(5):788-96 [10787439.001]
  • [Cites] Prog Lipid Res. 2000 May;39(3):257-88 [10799718.001]
  • [Cites] Anal Biochem. 2000 Nov 15;286(2):214-23 [11067743.001]
  • [Cites] Biochemistry. 2005 Jan 18;44(2):462-70 [15641770.001]
  • [Cites] Biochemistry. 2005 Jun 14;44(23):8251-9 [15938614.001]
  • [Cites] Neurology. 2005 Jun 28;64(12):2040-5 [15985568.001]
  • [Cites] J Neurochem. 2005 Aug;94(3):839-49 [16033426.001]
  • [Cites] J Neurochem. 2004 Mar;88(5):1168-78 [15009672.001]
  • [Cites] J Mol Biol. 2004 Apr 2;337(4):1001-9 [15033366.001]
  • [Cites] Am J Med Genet A. 2004 May 1;126A(4):349-54 [15098233.001]
  • [Cites] J Biol Chem. 2004 Jun 4;279(23):23882-91 [15051725.001]
  • [Cites] Prog Lipid Res. 2004 Jul;43(4):350-80 [15234552.001]
  • [Cites] J Biol Chem. 2004 Aug 13;279(33):34481-8 [15194696.001]
  • [Cites] J Lipid Res. 2004 Sep;45(9):1777-82 [15210839.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 12;101(41):14966-71 [15465911.001]
  • [Cites] Biochem Cell Biol. 2004 Oct;82(5):569-76 [15499385.001]
  • [Cites] Biochim Biophys Acta. 1970 Jun 9;210(1):15-27 [5456034.001]
  • [Cites] Anal Biochem. 1978 Oct 1;90(1):420-6 [727482.001]
  • [Cites] Biochem J. 1979 Feb 15;178(2):415-26 [220964.001]
  • [Cites] Biochim Biophys Acta. 1982 Dec 8;693(1):105-12 [6295475.001]
  • [Cites] Biochim Biophys Acta. 1982 Dec 8;693(1):113-24 [6295476.001]
  • [Cites] Nucleic Acids Res. 1988 Feb 11;16(3):1215 [3344216.001]
  • [Cites] Annu Rev Nutr. 1988;8:517-41 [3060176.001]
  • [Cites] J Neurochem. 1990 Mar;54(3):823-7 [2154550.001]
  • [Cites] J Nutr. 1991 Oct;121(10):1548-53 [1765818.001]
  • [Cites] J Neurochem. 1992 Aug;59(2):487-91 [1629722.001]
  • [Cites] FEBS Lett. 1992 Oct 19;311(2):107-9 [1327877.001]
  • [Cites] Brain Res Brain Res Rev. 1992 Sep-Dec;17(3):187-214 [1467810.001]
  • [Cites] J Biol Chem. 1993 Jul 25;268(21):15442-54 [8340373.001]
  • [Cites] J Biol Chem. 1993 Oct 25;268(30):22914-9 [8226801.001]
  • [Cites] J Biol Chem. 1994 Jul 8;269(27):17784-93 [8027032.001]
  • [Cites] Am J Physiol. 1994 Aug;267(2 Pt 1):C313-39 [8074170.001]
  • [Cites] Lipids. 1996 Jun;31(6):611-6 [8784741.001]
  • [Cites] Arch Biochem Biophys. 1997 May 1;341(1):112-21 [9143360.001]
  • [Cites] J Neurochem. 1997 Dec;69(6):2564-70 [9375690.001]
  • [Cites] J Neurochem. 1998 Mar;70(3):1227-34 [9489745.001]
  • [Cites] Biophys J. 1998 Feb;74(2 Pt 1):879-91 [9533699.001]
  • [Cites] Biochemistry. 1998 Apr 7;37(14):4901-9 [9538008.001]
  • [Cites] J Biol Chem. 1998 Apr 17;273(16):9443-9 [9545270.001]
  • [Cites] J Biol Chem. 1998 May 22;273(21):12753-7 [9582300.001]
  • [Cites] Trends Neurosci. 1998 Jun;21(6):249-54 [9641537.001]
  • [Cites] J Biol Chem. 1957 May;226(1):497-509 [13428781.001]
  • [Cites] Methods Cell Biol. 2001;65:75-96 [11381611.001]
  • [Cites] Methods Cell Biol. 2001;65:97-117 [11381612.001]
  • [Cites] J Mol Neurosci. 2001 Apr-Jun;16(2-3):87-92; discussion 151-7 [11478388.001]
  • [Cites] J Mol Neurosci. 2001 Apr-Jun;16(2-3):109-15; discussion 151-7 [11478365.001]
  • [Cites] J Mol Neurosci. 2001 Apr-Jun;16(2-3):133-42; discussion 151-7 [11478368.001]
  • [Cites] J Mol Neurosci. 2001 Apr-Jun;16(2-3):159-65; discussion 215-21 [11478370.001]
  • [Cites] J Mol Neurosci. 2001 Apr-Jun;16(2-3):167-72; discussion 215-21 [11478371.001]
  • [Cites] J Mol Neurosci. 2001 Apr-Jun;16(2-3):181-93; discussion 215-21 [11478373.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jul 31;98(16):9110-5 [11481478.001]
  • [Cites] FEBS Lett. 2001 Dec 7;509(2):151-5 [11741580.001]
  • [Cites] J Biol Chem. 2002 Feb 22;277(8):6344-52 [11744721.001]
  • [Cites] J Neurochem. 2002 Mar;80(5):780-7 [11948241.001]
  • [Cites] J Neurosci. 2002 Oct 15;22(20):8797-807 [12388586.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14524-9 [12376616.001]
  • [Cites] J Biol Chem. 2002 Nov 15;277(46):43553-6 [12364341.001]
  • [Cites] J Lipid Res. 2003 Jan;44(1):109-17 [12518029.001]
  • [Cites] Mol Cell. 2003 Mar;11(3):807-15 [12667461.001]
  • [Cites] Biochim Biophys Acta. 2003 Jun 10;1632(1-3):72-9 [12782153.001]
  • [Cites] Science. 2003 Oct 31;302(5646):819-22 [14593166.001]
  • [Cites] Biochemistry. 2003 Nov 11;42(44):12919-26 [14596606.001]
  • [Cites] J Biol Chem. 2003 Dec 12;278(50):49874-81 [14507911.001]
  • [Cites] J Biol Chem. 2003 Dec 19;278(51):51380-5 [14551214.001]
  • [Cites] J Biol Chem. 2003 Dec 26;278(52):52873-80 [14561769.001]
  • [Cites] Neurobiol Aging. 2005 Jan;26(1):25-35 [15585343.001]
  • [Cites] Neuron. 2000 Jan;25(1):239-52 [10707987.001]
  • (PMID = 16260631.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / 1R21 NS043697-01A; United States / PHS HHS / / 5P20R01-7699-02; United States / NINDS NIH HHS / NS / R21 NS043697; United States / Intramural NIH HHS / / ; United States / NHGRI NIH HHS / HG / Z01 HG000117-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cardiolipins; 0 / Fatty Acids; 0 / Lipids; 0 / Phosphatidylglycerols; 0 / Phospholipids; 0 / alpha-Synuclein; 1720-32-7 / Diphenylhexatriene; 27YG812J1I / Arachidonic Acid; 2V16EO95H1 / Palmitic Acid
  • [Other-IDs] NLM/ PMC1280279
  •  go-up   go-down


98. Kalivendi SV, Yedlapudi D, Hillard CJ, Kalyanaraman B: Oxidants induce alternative splicing of alpha-synuclein: Implications for Parkinson's disease. Free Radic Biol Med; 2010 Feb 1;48(3):377-83
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oxidants induce alternative splicing of alpha-synuclein: Implications for Parkinson's disease.
  • alpha-Synuclein (alpha-syn) is a presynaptic protein that is widely implicated in the pathophysiology of Parkinson's disease (PD).
  • Emerging evidence indicates a strong correlation between alpha-syn aggregation and proteasomal dysfunction as one of the major pathways responsible for destruction of the dopamine neurons.
  • Using parkinsonism mimetics (MPP(+), rotenone) and related oxidants, we have identified an oxidant-induced alternative splicing of alpha-syn mRNA, generating a shorter isoform of alpha-syn with deleted exon-5 (112-syn).
  • We conclude that oxidant-induced alternative splicing of alpha-syn plays a crucial role in the mechanism of dopamine neuron cell death and thus contributes to PD.

  • MedlinePlus Health Information. consumer health - Parkinson's Disease.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE .
  • Hazardous Substances Data Bank. ROTENONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009. Published by Elsevier Inc.
  • (PMID = 19857570.001).
  • [ISSN] 1873-4596
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS039958; United States / NINDS NIH HHS / NS / NS39958
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic Agents; 0 / Dopamine Agents; 0 / Oxidants; 0 / RNA, Messenger; 0 / Uncoupling Agents; 0 / alpha-Synuclein; 03L9OT429T / Rotenone; 8HW4YBZ748 / Oxidopamine; 9P21XSP91P / 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; EC 1.14.16.2 / Tyrosine 3-Monooxygenase
  • [Other-IDs] NLM/ NIHMS640838; NLM/ PMC4485429
  •  go-up   go-down


99. Kan SH, Mancini G, Gallagher G: Identification and characterization of multiple splice forms of the human interleukin-23 receptor alpha chain in mitogen-activated leukocytes. Genes Immun; 2008 Oct;9(7):631-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification and characterization of multiple splice forms of the human interleukin-23 receptor alpha chain in mitogen-activated leukocytes.
  • Twenty-four different IL23R transcripts were observed in this study, which may potentially lead to an alteration in the protein coding region of IL-23R alpha.
  • Consequently, by analysing amino acid sequences deduced from alternatively spliced mRNA sequences, four different putative premature early termination forms of IL-23R alpha:.
  • (1) a very short 'IL-23R alpha', (2) an IL-23R alpha containing only the extracellular region, (3) a IL-23R alpha with truncated intracellular domain and (4) in-frame exon-skipping causing changes to the extracellular region of the IL-23R alpha were revealed.
  • These changes may affect the function of IL-23R by altering the ligand-binding interaction, producing a soluble form of the receptor to act as a decoy receptor and/or modify the IL-23/IL-23R signalling, respectively.
  • [MeSH-minor] Cells, Cultured. Crohn Disease / genetics. Crohn Disease / immunology. Genetic Predisposition to Disease. Genetic Variation. Humans. Lymphocyte Activation / genetics. Protein Isoforms / biosynthesis. Protein Isoforms / chemistry. Protein Isoforms / genetics. Protein Subunits / biosynthesis. Protein Subunits / chemistry. Protein Subunits / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18754016.001).
  • [ISSN] 1476-5470
  • [Journal-full-title] Genes and immunity
  • [ISO-abbreviation] Genes Immun.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IL23R protein, human; 0 / Mitogens; 0 / Protein Isoforms; 0 / Protein Subunits; 0 / Receptors, Interleukin
  •  go-up   go-down


100. Wajcman H, Traeger-Synodinos J, Papassotiriou I, Giordano PC, Harteveld CL, Baudin-Creuza V, Old J: Unstable and thalassemic alpha chain hemoglobin variants: a cause of Hb H disease and thalassemia intermedia. Hemoglobin; 2008;32(4):327-49
Genetic Alliance. consumer health - Thalassemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unstable and thalassemic alpha chain hemoglobin variants: a cause of Hb H disease and thalassemia intermedia.
  • We report an update of the alpha-globin gene point mutations resulting in structural modification associated with an alpha-thalassemia (alpha-thal) phenotype.
  • These variants, barely symptomatic in the heterozygous state, are either unstable due to folding defects and/or defects in binding to alpha-hemoglobin stabilizing protein (AHSP).
  • This is predicted to result in precipitation of the unstable alpha chains or Hb variant, a concomitant decrease in the overall quantity of normal alpha-globin in the red cells and a potential degree of anemia and possibly, hemolysis.
  • Genotype/phenotype correlation and potential genetic risk in combination with common or less common alpha-thal defects are discussed.
  • [MeSH-major] Genetic Variation. Hemoglobins, Abnormal / genetics. alpha-Thalassemia / genetics

  • Genetic Alliance. consumer health - Hemoglobin H Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18654884.001).
  • [ISSN] 1532-432X
  • [Journal-full-title] Hemoglobin
  • [ISO-abbreviation] Hemoglobin
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins, Abnormal; 9004-22-2 / Globins
  • [Number-of-references] 82
  •  go-up   go-down






Advertisement