[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 91 of about 91
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. 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


5. 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


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. 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


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. 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


10. 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


11. 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


12. 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


13. 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


14. 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


15. 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


16. 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


17. 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


18. 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


19. 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


20. 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


21. 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


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. 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


24. 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


25. 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


26. 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


27. 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


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. Dyer MJ, Akasaka T, Capasso M, Dusanjh P, Lee YF, Karran EL, Nagel I, Vater I, Cario G, Siebert R: Immunoglobulin heavy chain locus chromosomal translocations in B-cell precursor acute lymphoblastic leukemia: rare clinical curios or potent genetic drivers? Blood; 2010 Feb 25;115(8):1490-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoglobulin heavy chain locus chromosomal translocations in B-cell precursor acute lymphoblastic leukemia: rare clinical curios or potent genetic drivers?
  • Chromosomal translocations involving the immunoglobulin heavy chain (IGH) locus define common subgroups of B-cell lymphoma but are rare in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
  • The possible clinical importance of many of the various IGH translocations in BCP-ALL remains to be determined from prospective studies, but CRLF2 expression is associated with a poor prognosis.
  • Despite their rarity, IGH chromosomal translocations in BCP-ALL therefore define not only new mechanisms of B-cell transformation but also clinically important subgroups of disease and suggest new targeted therapeutic approaches.
  • [MeSH-major] B-Lymphocytes / metabolism. Cell Transformation, Neoplastic / metabolism. Immunoglobulin Heavy Chains / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Quantitative Trait Loci. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Animals. Core Binding Factor Alpha 2 Subunit / biosynthesis. Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Leukemic / genetics. Hematopoiesis / genetics. Humans. Inhibitor of Differentiation Proteins / biosynthesis. Inhibitor of Differentiation Proteins / genetics. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Prognosis. Receptors, Cytokine / biosynthesis. Receptors, Cytokine / genetics. Receptors, Erythropoietin / biosynthesis. Receptors, Erythropoietin / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20042721.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670597
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CRLF2 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / ID4 protein, human; 0 / Immunoglobulin Heavy Chains; 0 / Inhibitor of Differentiation Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Cytokine; 0 / Receptors, Erythropoietin; 0 / TEL-AML1 fusion protein
  • [Number-of-references] 87
  •  go-up   go-down


31. Song J, Patel M, Rosenzweig CN, Chan-Li Y, Sokoll LJ, Fung ET, Choi-Miura NH, Goggins M, Chan DW, Zhang Z: Quantification of fragments of human serum inter-alpha-trypsin inhibitor heavy chain 4 by a surface-enhanced laser desorption/ionization-based immunoassay. Clin Chem; 2006 Jun;52(6):1045-53
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] Quantification of fragments of human serum inter-alpha-trypsin inhibitor heavy chain 4 by a surface-enhanced laser desorption/ionization-based immunoassay.
  • BACKGROUND: Several proteolytically derived fragments from the proline-rich region (PRR) of human inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) have been identified by surface-enhanced or matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS or MALDI-TOF-MS) as potential disease markers.
  • In this study, we used this high-throughput approach to quantify and characterize the extensive fragmentation within the PRR of human serum ITIH4 and determined its association with different disease conditions.
  • RESULTS: Human serum ITIH4 was shown to be extensively proteolytically processed within the PRR, and its fragmentation patterns were closely associated with different disease conditions.
  • CONCLUSIONS: The fragmentation patterns within the PRR of human serum ITIH4 are associated with different disease conditions and may hold important diagnostic information.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16574760.001).
  • [ISSN] 0009-9147
  • [Journal-full-title] Clinical chemistry
  • [ISO-abbreviation] Clin. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1P50 CA83639; United States / NCI NIH HHS / CA / CA115102-01; United States / NCI NIH HHS / CA / CA62924
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Blood Proteins; 0 / Glycoproteins; 0 / ITIH4 protein, human; 0 / Proteinase Inhibitory Proteins, Secretory
  •  go-up   go-down


32. Budde BS, Binner P, Waldmüller S, Höhne W, Blankenfeldt W, Hassfeld S, Brömsen J, Dermintzoglou A, Wieczorek M, May E, Kirst E, Selignow C, Rackebrandt K, Müller M, Goody RS, Vosberg HP, Nürnberg P, Scheffold T: Noncompaction of the ventricular myocardium is associated with a de novo mutation in the beta-myosin heavy chain gene. PLoS One; 2007;2(12):e1362

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Noncompaction of the ventricular myocardium is associated with a de novo mutation in the beta-myosin heavy chain gene.
  • Noncompaction of the ventricular myocardium (NVM) is the morphological hallmark of a rare familial or sporadic unclassified heart disease of heterogeneous origin.
  • For molecular characterization, a genome-wide linkage analysis was undertaken and the disease locus was mapped to chromosome 14ptel-14q12.
  • Subsequently, two genes of the disease interval, MYH6 and MYH7 (encoding the alpha- and beta-myosin heavy chain, respectively) were sequenced, leading to the identification of a previously unknown de novo missense mutation, c.842G>C, in the gene MYH7.
  • A high degree of clinical variability was observed, ranging from the absence of symptoms in childhood to cardiac death in the third decade of life.
  • [MeSH-major] Heart Ventricles / metabolism. Mutation, Missense. Myosin Heavy Chains / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Mol Cell Cardiol. 2003 Jun;35(6):623-36 [12788380.001]
  • [Cites] Cardiology. 2002;98(1-2):25-32 [12373044.001]
  • [Cites] J Am Coll Cardiol. 2003 Dec 3;42(11):2014-27 [14662268.001]
  • [Cites] Circulation. 2004 Jun 8;109(22):2720-3 [15173023.001]
  • [Cites] Am J Cardiol. 1984 Jun 1;53(11):1733-4 [6731322.001]
  • [Cites] J Clin Invest. 1988 Aug;82(2):524-31 [2969919.001]
  • [Cites] Circulation. 1990 Aug;82(2):507-13 [2372897.001]
  • [Cites] Genomics. 1990 Oct;8(2):194-206 [2249844.001]
  • [Cites] Nucleic Acids Res. 1991 Jul 25;19(14):4019 [1862006.001]
  • [Cites] Circ Res. 1992 Jul;71(1):3-8 [1606666.001]
  • [Cites] Science. 1993 Jul 2;261(5117):50-8 [8316857.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Apr 25;92(9):3864-8 [7731997.001]
  • [Cites] Circulation. 1996 Mar 1;93(5):841-2 [8598070.001]
  • [Cites] Am J Hum Genet. 1996 Jun;58(6):1323-37 [8651310.001]
  • [Cites] Am J Hum Genet. 1997 Oct;61(4):868-72 [9382097.001]
  • [Cites] J Am Coll Cardiol. 1999 Jul;34(1):233-40 [10400016.001]
  • [Cites] Am J Med Genet. 1999 Aug 6;85(4):419-23 [10398271.001]
  • [Cites] Eur Heart J. 2005 Jan;26(2):187-92 [15618076.001]
  • [Cites] Bioinformatics. 2005 Feb 1;21(3):405-7 [15347576.001]
  • [Cites] Eur Heart J. 2005 Apr;26(8):794-803 [15769782.001]
  • [Cites] Nat Genet. 2005 Apr;37(4):423-8 [15735645.001]
  • [Cites] J Cardiovasc Electrophysiol. 2005 Aug;16(8):927-35 [16101641.001]
  • [Cites] Nat Genet. 2006 Mar;38(3):343-9 [16444274.001]
  • [Cites] Circulation. 2006 Apr 11;113(14):1807-16 [16567565.001]
  • [Cites] Nat Genet. 2006 May;38(5):561-5 [16642020.001]
  • [Cites] Expert Rev Cardiovasc Ther. 2006 Nov;4(6):927-34 [17173506.001]
  • [Cites] Ann Med. 2007;39(2):91-107 [17453673.001]
  • [Cites] Anat Rec. 2000 Apr 1;258(4):319-37 [10737851.001]
  • [Cites] Circulation. 2001 Mar 6;103(9):1256-63 [11238270.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2001 Apr;280(4):H1814-20 [11247796.001]
  • [Cites] Heart. 2001 Dec;86(6):666-71 [11711464.001]
  • [Cites] Heart. 2003 Oct;89(10):1179-85 [12975413.001]
  • (PMID = 18159245.001).
  • [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] EC 3.6.4.1 / Myosin Heavy Chains
  • [Other-IDs] NLM/ PMC2137931
  •  go-up   go-down


33. Kim SK, Park IK, Park BH, Park W, Lee HS, Kim TH, Jun JB, Bae SC, Yoo DH, Uhm WS: A case report: isolated a heavy chain monoclonal gammopathy in a patient with polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin change syndrome. Int J Clin Pract Suppl; 2005 Apr;(147):26-30

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case report: isolated a heavy chain monoclonal gammopathy in a patient with polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin change syndrome.
  • A 45-year-old South-Korean man presented with abdominal distension, progressive paresthesia and motor weakness of both lower extremities.
  • Circulating M components of POEMS syndrome consist mainly of IgG or IgA-lambda and rarely IgM-lambda, IgG-kappa or isolated light chains.
  • In this case, the M-band on serum protein electrophoresis and isolated IgA heavy chain on serum immunofixation electrophoresis were demonstrated, but there was no abnormal light chain.
  • We suggest that this case may be associated with a pattern of abnormal secretion of monoclonal protein or a coincidence of a heavy chain disease in POEMS syndrome, even though the latter possibility may be very rare.
  • [MeSH-major] Heavy Chain Disease / diagnosis. POEMS Syndrome / diagnosis
  • [MeSH-minor] Bone Marrow / radionuclide imaging. Humans. Immunoglobulin A / blood. Immunoglobulin alpha-Chains / blood. Male. Middle Aged. Pleural Effusion / radiography. Pulmonary Atelectasis / radiography

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15875614.001).
  • [ISSN] 1368-504X
  • [Journal-full-title] International journal of clinical practice. Supplement
  • [ISO-abbreviation] Int J Clin Pract Suppl
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin A; 0 / Immunoglobulin alpha-Chains
  •  go-up   go-down


34. Liao PC, Yu L, Kuo CC, Lin C, Kuo YM: Proteomics analysis of plasma for potential biomarkers in the diagnosis of Alzheimer's disease. Proteomics Clin Appl; 2007 May;1(5):506-12
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] Proteomics analysis of plasma for potential biomarkers in the diagnosis of Alzheimer's disease.
  • The objective of this study was to search for biological markers associated with Alzheimer's disease (AD).
  • Plasma specimens obtained from ten pathologically diagnosed AD patients and ten non-demented (ND) control subjects were analyzed by a combination of 2-DE and MS.
  • This strategy allowed us to identify six plasma proteins (alpha-1-antitrypsin, vitamin D-binding protein, inter-alpha-trypsin inhibitor family heavy chain-related protein, apolipoprotein J precursor, cAMP-dependent protein kinase catalytic subunit alpha 1, and an orf) whose 2-DE spot densities were different between the AD and ND groups.
  • Due to their involvements in AD amyloid plaque formation, the plasma concentrations of alpha-1-antitrypsin and apolipoprotein J were further validated using either ELISA or Western blot.
  • The results revealed that the plasma levels of alpha-1-antitrypsin in AD were higher than those of controls, confirming the 2-DE findings.
  • Considering the difference in resolving power to differentially quantitate protein isoforms provided by 2-DE and Western blot, 2-DE analysis combined with MS protein identification offers distinctive advantages when a disease-related protein isoform-specific variance is investigated.

  • COS Scholar Universe. author profiles.
  • 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
  • [Copyright] Copyright © 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
  • (PMID = 21136702.001).
  • [ISSN] 1862-8346
  • [Journal-full-title] Proteomics. Clinical applications
  • [ISO-abbreviation] Proteomics Clin Appl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


35. 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


36. Shaye OS, Levine AM: Marginal zone lymphoma. J Natl Compr Canc Netw; 2006 Mar;4(3):311-8
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Marginal zone lymphoma.
  • Marginal zone lymphomas (MZLs) comprise 3 distinct entities: extranodal MZL of mucosa-associated lymphoid tissue (MALT), splenic MZL, and nodal MZL.
  • Gastric MALT lymphoma is the most common extranodal MZL and often develops as a result of chronic Helicobacter pylori gastritis.
  • Antigen-driven lymphomatous disease can also be seen in the association of Borrelia burgdorferi with MALT lymphoma of the skin, Chlamydia psittaci with MALT lymphoma of the ocular adnexa, Campylobacter jejuni with immunoproliferative disease of the small intestine, and hepatitis C with splenic MZL.
  • This article discusses the pathogenesis and clinical features of MZL and the treatment options available to patients.
  • [MeSH-major] Helicobacter Infections / complications. Lymphoma / diagnosis. Lymphoma / therapy. Splenic Neoplasms. Stomach Neoplasms
  • [MeSH-minor] Chronic Disease. Gastritis / microbiology. Helicobacter pylori. Humans. Lymphoma, B-Cell, Marginal Zone

  • MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16507274.001).
  • [ISSN] 1540-1405
  • [Journal-full-title] Journal of the National Comprehensive Cancer Network : JNCCN
  • [ISO-abbreviation] J Natl Compr Canc Netw
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 73
  •  go-up   go-down


37. Zelarayan L, Renger A, Noack C, Zafiriou MP, Gehrke C, van der Nagel R, Dietz R, de Windt L, Bergmann MW: NF-kappaB activation is required for adaptive cardiac hypertrophy. Cardiovasc Res; 2009 Dec 1;84(3):416-24
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.
  • METHODS AND RESULTS: Cardiac-restricted NF-kappaB inhibition was achieved by expression of a stabilized IkappaBalpha mutant (IkappaBalphaDeltaN) in cells with an active alpha-myosin heavy chain (alphaMHC) promoter employing the Cre/lox technique.
  • [MeSH-minor] Angiotensin II / metabolism. Animals. Apoptosis / physiology. Disease Models, Animal. Female. Fibrosis. I-kappa B Proteins / genetics. I-kappa B Proteins / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Mutation / genetics. Myocardium / metabolism. Myocardium / pathology. Myocytes, Cardiac / metabolism. Myocytes, Cardiac / pathology. Myosin Heavy Chains / metabolism. Receptor, Angiotensin, Type 1 / physiology. Signal Transduction / physiology

  • 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 = 19620128.001).
  • [ISSN] 1755-3245
  • [Journal-full-title] Cardiovascular research
  • [ISO-abbreviation] Cardiovasc. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Receptor, Angiotensin, Type 1; 11128-99-7 / Angiotensin II; 139874-52-5 / NF-kappaB inhibitor alpha; EC 3.6.4.1 / Myosin Heavy Chains
  •  go-up   go-down


38. Stauffer BL, Konhilas JP, Luczak ED, Leinwand LA: Soy diet worsens heart disease in mice. J Clin Invest; 2006 Jan;116(1):209-16
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] Soy diet worsens heart disease in mice.
  • We report that dietary modification from a soy-based diet to a casein-based diet radically improves disease indicators and cardiac function in a transgenic mouse model of hypertrophic cardiomyopathy.
  • On a soy diet, males with a mutation in the alpha-myosin heavy chain gene progress to dilation and heart failure.
  • Further, this diet prevents a number of pathologic indicators in males, including fibrosis, induction of beta-myosin heavy chain, inactivation of glycogen synthase kinase 3beta (GSK3beta), and caspase-3 activation.

  • MedlinePlus Health Information. consumer health - Heart Disease in Women.
  • MedlinePlus Health Information. consumer health - Heart Diseases.
  • COS Scholar Universe. author profiles.
  • 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] Am J Physiol Heart Circ Physiol. 2001 Sep;281(3):H1217-22 [11514290.001]
  • [Cites] Endocrinology. 2000 Dec;141(12):4503-11 [11108261.001]
  • [Cites] J Biol Chem. 2002 Mar 8;277(10):8531-7 [11751931.001]
  • [Cites] J Biol Chem. 2002 Jun 21;277(25):22896-901 [11943770.001]
  • [Cites] J Cell Biol. 2000 Oct 2;151(1):117-30 [11018058.001]
  • [Cites] Reprod Toxicol. 2004 Jul;18(5):677-85 [15219630.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2001 Jan;280(1):H151-9 [11123229.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2001 Mar;280(3):H1136-44 [11179057.001]
  • [Cites] Arch Intern Med. 2001 May 14;161(9):1161-72 [11343439.001]
  • [Cites] Lab Invest. 2001 May;81(5):735-47 [11351045.001]
  • [Cites] Biol Cell. 2000 Dec;92(8-9):595-604 [11374438.001]
  • [Cites] Circ Res. 2001 May 25;88(10):1020-7 [11375271.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 22;99(2):907-12 [11782539.001]
  • [Cites] Endocrinology. 1974 Jun;94(6):1704-8 [4857496.001]
  • [Cites] J Nutr. 1977 Jul;107(7):1340-8 [874577.001]
  • [Cites] Biol Reprod. 1979 Apr;20(3):659-70 [572241.001]
  • [Cites] Circulation. 1981 Feb;63(2):360-71 [6450003.001]
  • [Cites] Circ Res. 1984 Jan;54(1):38-49 [6229365.001]
  • [Cites] Jpn Circ J. 1984 May;48(5):445-56 [6539397.001]
  • [Cites] Physiol Rev. 1986 Jul;66(3):710-71 [2942954.001]
  • [Cites] Steroids. 1985 Jul;46(1):587-608 [3837406.001]
  • [Cites] Br Heart J. 1987 Sep;58(3):259-66 [3663427.001]
  • [Cites] Circ Res. 1989 Jun;64(6):1041-50 [2524288.001]
  • [Cites] Am J Physiol. 1990 Sep;259(3 Pt 2):H866-71 [2144404.001]
  • [Cites] Circulation. 1993 Jul;88(1):107-15 [8319323.001]
  • [Cites] Am J Cardiol. 1993 Aug 1;72(3):310-3 [8342510.001]
  • [Cites] Circ Res. 1995 Sep;77(3):544-55 [7641324.001]
  • [Cites] J Am Coll Cardiol. 1995 Oct;26(4):1068-79 [7560601.001]
  • [Cites] Cardiology. 1995;86(4):310-7 [7553706.001]
  • [Cites] Mol Med. 1996 Sep;2(5):556-67 [8898372.001]
  • [Cites] Circulation. 1996 Dec 1;94(11):2837-42 [8941110.001]
  • [Cites] J Gen Physiol. 1997 Aug;110(2):135-40 [9236206.001]
  • [Cites] FEBS Lett. 1997 Oct 13;416(1):107-12 [9369244.001]
  • [Cites] Proc Soc Exp Biol Med. 1998 Mar;217(3):300-9 [9492339.001]
  • [Cites] Environ Health Perspect. 1998 Jul;106(7):369-73 [9637793.001]
  • [Cites] Circulation. 1998 Jul 21;98(3):256-61 [9697826.001]
  • [Cites] Science. 1998 Aug 28;281(5381):1312-6 [9721091.001]
  • [Cites] Am J Physiol. 1998 Dec;275(6 Pt 2):R1968-76 [9843886.001]
  • [Cites] Am J Clin Nutr. 1998 Dec;68(6 Suppl):1333S-1346S [9848496.001]
  • [Cites] Environ Health Perspect. 1999 Apr;107(4):A182-3 [10383244.001]
  • [Cites] J Mol Cell Cardiol. 1999 Aug;31(8):1527-37 [10423350.001]
  • [Cites] Am J Cardiol. 1999 Sep 1;84(5):611-2, A9 [10482169.001]
  • [Cites] Circulation. 2005 Feb 1;111(4):385-7 [15687122.001]
  • [Cites] Circulation. 2005 Feb 1;111(4):465-71 [15687135.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2004;5:71-118 [15485344.001]
  • [Cites] Lab Anim Sci. 1999 Oct;49(5):530-6 [10551455.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2000 Feb;278(2):H412-9 [10666070.001]
  • [Cites] Microsc Res Tech. 2000 Sep 15;50(6):522-31 [10998641.001]
  • [Cites] Life Sci. 2002 Jul 12;71(8):865-77 [12084384.001]
  • [Cites] JAMA. 2002 Jul 17;288(3):321-33 [12117397.001]
  • [Cites] J Chromatogr B Analyt Technol Biomed Life Sci. 2002 Sep 25;777(1-2):269-79 [12270219.001]
  • [Cites] N Engl J Med. 2002 Oct 31;347(18):1397-402 [12409541.001]
  • [Cites] Cardiovasc Res. 2003 Feb;57(2):388-94 [12566111.001]
  • [Cites] Cell Mol Biol Lett. 2003;8(1):49-53 [12655356.001]
  • [Cites] Am J Med. 2003 Apr 15;114(6):470-6 [12727580.001]
  • [Cites] J Nutr. 2003 May;133(5):1238-43 [12730403.001]
  • [Cites] Endocrinology. 2003 Sep;144(9):4097-105 [12933684.001]
  • [Cites] Circ Res. 2004 Feb 6;94(2):201-7 [14670849.001]
  • [Cites] JAMA. 2004 Apr 14;291(14):1701-12 [15082697.001]
  • [Cites] Phytochemistry. 2004 Apr;65(8):995-1016 [15110680.001]
  • [Cites] J Nutr. 2004 May;134(5):1225S-1228S [15113976.001]
  • [Cites] Life Sci. 2004 Jun 11;75(4):499-509 [15147835.001]
  • [Cites] Mol Cell Endocrinol. 2004 May 31;220(1-2):51-8 [15196699.001]
  • [CommentIn] J Clin Invest. 2006 Jan;116(1):16-9 [16395397.001]
  • (PMID = 16395406.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL067543-01; United States / NHLBI NIH HHS / HL / 1F32HL67543; United States / NIGMS NIH HHS / GM / T32 GM008759; United States / NHLBI NIH HHS / HL / F32 HL067543-01; United States / NHLBI NIH HHS / HL / F32 HL067543; United States / NHLBI NIH HHS / HL / 5F32HL070509; United States / NHLBI NIH HHS / HL / R01 HL050560; United States / NHLBI NIH HHS / HL / 2R01HL050560; United States / NHLBI NIH HHS / HL / F32 HL070509
  • [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 / Soybean Proteins; EC 3.6.4.1 / Myosin Heavy Chains
  • [Other-IDs] NLM/ PMC1323247
  •  go-up   go-down


39. North KN, Laing NG: Skeletal muscle alpha-actin diseases. Adv Exp Med Biol; 2008;642:15-27
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Skeletal muscle alpha-actin diseases.
  • Skeletal muscle alpha-actin is the principal protein component of the adult skeletal muscle thin filament.
  • The interaction between skeletal muscle alpha-actin and the various myosin heavy chain proteins in the different muscle fibre types generates the force of muscle contraction.
  • Skeletal muscle alpha-alpha actin is thus of fundamental importance to normal muscle contraction.
  • To date over 140 different disease-causing mutations have been identified in the skeletal muscle alpha-actin gene ACTA1.
  • These mutations are associated with histologically distinct congenital myopathies, including nemaline myopathy, actin myopathy, intranuclear rod myopathy, congenital fibre type disproportion and myopathy with cores.
  • Mutations in ACTA1 are associated with a wide range of clinical severity although the majority of patients tend to have severe congenital-onset disease.
  • Most of the patients have de novo dominant mutations not present in either parent.
  • However mild ACTA1 disease may be dominantly inherited and there are also recessive mutations.
  • Information from the clinic suggests that exercise and L-tyrosine may benefit some patients and that in the future decreasing the proportion of mutant actin may ameliorate the disease in some patients.
  • [MeSH-major] Actins / metabolism. Muscular Diseases / metabolism

  • MedlinePlus Health Information. consumer health - Muscle Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19181090.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins
  •  go-up   go-down


40. Berentsen S, Beiske K, Tjønnfjord GE: Primary chronic cold agglutinin disease: an update on pathogenesis, clinical features and therapy. Hematology; 2007 Oct;12(5):361-70
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] Primary chronic cold agglutinin disease: an update on pathogenesis, clinical features and therapy.
  • Chronic cold agglutinin disease (CAD) is a subgroup of autoimmune hemolytic anemia.
  • Primary CAD has traditionally been defined by the absence of any underlying or associated disease.
  • The results of therapy with corticosteroids, alkylating agents and interferon-alpha have been poor.
  • These cold agglutinins are monoclonal, usually IgMkappa autoantibodies with heavy chain variable regions encoded by the V(H)4-34 gene segment.
  • By flowcytometric and immunohistochemical assessments, a monoclonal CD20+kappa+B-lymphocyte population has been demonstrated in the bone marrow of 90% of the patients, and lymphoplasmacytic lymphoma is a frequent finding.
  • In this review, we discuss the clinical and pathogenetic features of primary CAD, emphasizing the more recent data on its close association with clonal lymphoproliferative bone marrow disorders and implications for therapy.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Alkylating Agents / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. B-Lymphocytes / pathology. Bone Marrow / pathology. Clone Cells / pathology. Cryoglobulins / analysis. Cryoglobulins / immunology. Humans. Immunotherapy. Interferon-alpha / therapeutic use. Lymphoproliferative Disorders / complications. Lymphoproliferative Disorders / drug therapy. Lymphoproliferative Disorders / pathology. Rituximab

  • Genetic Alliance. consumer health - Cold Agglutinin Disease.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. RITUXIMAB .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Hematol. 2002 Apr;69(4):258-71 [11921020.001]
  • [Cites] Rev Med Interne. 2002 Nov;23(11):901-9 [12481390.001]
  • [Cites] J Allergy Clin Immunol. 2003 Apr;111(4):697-703 [12704346.001]
  • [Cites] Semin Oncol. 2003 Apr;30(2):110-5 [12720118.001]
  • [Cites] Semin Oncol. 2003 Apr;30(2):239-42 [12720144.001]
  • [Cites] Semin Oncol. 2003 Apr;30(2):243-7 [12720145.001]
  • [Cites] Semin Oncol. 2003 Apr;30(2):318-24 [12720161.001]
  • [Cites] Rev Med Interne. 2003 Aug;24(8):501-4 [12888170.001]
  • [Cites] Scand J Immunol. 2004 Jan;59(1):103-8 [14723628.001]
  • [Cites] Blood. 2004 Apr 15;103(8):2925-8 [15070665.001]
  • [Cites] Cancer Genet Cytogenet. 2004 Jul 1;152(1):66-9 [15193444.001]
  • [Cites] Am J Hematol. 1996 Dec;53(4):279-80 [8948674.001]
  • [Cites] APMIS. 1997 May;105(5):354-62 [9201236.001]
  • [Cites] J Clin Oncol. 1997 Oct;15(10):3266-74 [9336364.001]
  • [Cites] Transfusion. 1997 Nov-Dec;37(11-12):1111-6 [9426632.001]
  • [Cites] Eur J Haematol. 1998 Feb;60(2):93-100 [9508349.001]
  • [Cites] Ann Hematol. 1998 May;76(5):201-4 [9671133.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2825-33 [9704735.001]
  • [Cites] J Immunol. 1998 Oct 15;161(8):4091-7 [9780180.001]
  • [Cites] Blood. 1998 Nov 1;92(9):3490-1 [9787200.001]
  • [Cites] Eur J Haematol. 1999 Oct;63(4):259-66 [10530415.001]
  • [Cites] Acta Med Scand. 1954;148(4):299-308 [13157944.001]
  • [Cites] Scand J Immunol. 2000 Jun;51(6):634-41 [10849376.001]
  • [Cites] Transfus Sci. 2000 Feb-Apr;22(1-2):113-9 [10771399.001]
  • [Cites] Eur J Haematol. 2000 Jul;65(1):88-90 [10914950.001]
  • [Cites] Cytokines Cell Mol Ther. 2000 Jun;6(2):81-7 [11108573.001]
  • [Cites] Scand J Immunol. 2001 Jul-Aug;54(1-2):239-42 [11439172.001]
  • [Cites] Blood. 2004 Oct 1;104(7):2134-42 [14764523.001]
  • [Cites] Scand J Haematol. 1965;2(3):259-66 [4158055.001]
  • [Cites] Semin Hematol. 1966 Jan;3(1):27-47 [5323366.001]
  • [Cites] Scand J Clin Lab Invest. 1966;18(1):1-15 [5918670.001]
  • [Cites] Scand J Haematol. 1969;6(6):416-26 [4984643.001]
  • [Cites] J Clin Invest. 1976 Oct;58(4):942-9 [965497.001]
  • [Cites] Br J Haematol. 1957 Jul;3(3):262-75 [13460195.001]
  • [Cites] J Exp Med. 1957 Nov 1;106(5):689-702 [13475624.001]
  • [Cites] Acta Med Scand. 1961 Dec;170:725-9 [14452388.001]
  • [Cites] Scand J Haematol. 1964;1:223-37 [14214902.001]
  • [Cites] Ann Intern Med. 1956 Feb;44(2):221-40 [13292836.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2004;:48-62 [15561676.001]
  • [Cites] J Clin Oncol. 2005 Jan 20;23(3):474-81 [15659493.001]
  • [Cites] Clin Lymphoma. 2005 Mar;5(4):261-4 [15794861.001]
  • [Cites] Leuk Lymphoma. 2006 Feb;47(2):253-60 [16321854.001]
  • [Cites] Clin Lab Haematol. 2006 Feb;28(1):57-9 [16430461.001]
  • [Cites] Haematologica. 2006 Feb;91(2):176-83 [16461301.001]
  • [Cites] Haematologica. 2006 Apr;91(4):439-41 [16585009.001]
  • [Cites] Haematologica. 2006 Apr;91(4):460-6 [16585012.001]
  • [Cites] N Engl J Med. 2006 Sep 21;355(12):1233-43 [16990386.001]
  • [Cites] Blood. 2006 Oct 15;108(8):2520-30 [16794250.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2006;:19-23 [17124034.001]
  • [Cites] Ann Oncol. 1996;7 Suppl 6:S27-33 [9010576.001]
  • [Cites] Am J Hematol. 1977;2(3):259-70 [596370.001]
  • [Cites] Cancer. 1978 Oct;42(4):1826-33 [101298.001]
  • [Cites] Blood. 1980 Sep;56(3):409-16 [7407408.001]
  • [Cites] Blood. 1981 Jan;57(1):189-91 [7448411.001]
  • [Cites] Br Med J (Clin Res Ed). 1981 Jun 20;282(6281):2023-7 [6788179.001]
  • [Cites] Am J Med. 1982 Jun;72(6):915-22 [6807086.001]
  • [Cites] Blood. 1986 Jun;67(6):1705-9 [3486685.001]
  • [Cites] Acta Haematol. 1988;79(1):20-5 [3124457.001]
  • [Cites] Ann Intern Med. 1989 Aug 1;111(3):255-6 [2502059.001]
  • [Cites] Eur J Immunol. 1990 Sep;20(9):1971-9 [2120070.001]
  • [Cites] Semin Hematol. 1991 Jan;28(1):66-77 [1708169.001]
  • [Cites] J Immunol. 1992 Oct 1;149(7):2337-44 [1382098.001]
  • [Cites] J Clin Invest. 1993 Dec;92(6):2821-33 [8254037.001]
  • [Cites] Blood. 1994 Jan 15;83(2):435-45 [7506951.001]
  • [Cites] Eur J Haematol. 1994 Oct;53(4):242-3 [7957810.001]
  • [Cites] Tidsskr Nor Laegeforen. 1995 Feb 10;115(4):473-5 [7871504.001]
  • [Cites] Infusionsther Transfusionsmed. 1994 Dec;21(6):405-9 [7873919.001]
  • [Cites] Infusionsther Transfusionsmed. 1994 Dec;21(6):410-5 [7873920.001]
  • [Cites] Br J Haematol. 1996 Jan;92(1):71-6 [8562414.001]
  • [Cites] N Engl J Med. 1996 Feb 15;334(7):437 [8552146.001]
  • [Cites] Br J Haematol. 2001 Sep;114(4):800-9 [11564066.001]
  • [Cites] Blood. 2001 Dec 1;98(12):3383-9 [11719378.001]
  • [Cites] Br J Haematol. 2001 Oct;115(1):79-83 [11722415.001]
  • [Cites] Blood. 2002 Feb 1;99(3):754-8 [11806974.001]
  • [Cites] Haematologica. 2002 Feb;87(2):113-4 [11836158.001]
  • (PMID = 17891600.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Alkylating Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Cryoglobulins; 0 / Interferon-alpha; 0 / cold agglutinins; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 88
  • [Other-IDs] NLM/ PMC2409172
  •  go-up   go-down


41. Ommen HB, Schnittger S, Jovanovic JV, Ommen IB, Hasle H, Østergaard M, Grimwade D, Hokland P: Strikingly different molecular relapse kinetics in NPM1c, PML-RARA, RUNX1-RUNX1T1, and CBFB-MYH11 acute myeloid leukemias. Blood; 2010 Jan 14;115(2):198-205
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.
  • Early relapse detection in acute myeloid leukemia is possible using standardized real-time quantitative polymerase chain reaction (RQ-PCR) protocols.
  • Furthermore, we used a mathematical model to determine frequency of relapse detection and median time from detection of minimal residual disease to hematologic relapse as a function of sampling interval length.
  • These data carry important implications for the development of optimal RQ-PCR monitoring schedules suitable for evaluation of minimal residual disease-directed therapies in future clinical trials.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Core Binding Factor Alpha 2 Subunit / biosynthesis. Core Binding Factor beta Subunit / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Myosin Heavy Chains / biosynthesis. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19901261.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFB protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / MYH11 protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 117896-08-9 / nucleophosmin; EC 3.6.4.1 / Myosin Heavy Chains
  •  go-up   go-down


42. Meurs KM, Norgard MM, Kuan M, Haggstrom J, Kittleson M: Analysis of 8 sarcomeric candidate genes for feline hypertrophic cardiomyopathy mutations in cats with hypertrophic cardiomyopathy. J Vet Intern Med; 2009 Jul-Aug;23(4):840-3
SciCrunch. OMIA - Online Mendelian Inheritance in Animals: Data: Gene Expression .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Hypertrophic cardiomyopathy (HCM) is the most common heart disease in cats.
  • Exonic and splice site regions of the genes encoding the proteins cardiac troponin I, troponin T, MYBPC3, cardiac essential myosin light chain, cardiac regulatory myosin light chain, alpha tropomyosin, actin, and beta-myosin heavy chain were sequenced.
  • CONCLUSIONS AND CLINICAL IMPORTANCE: Mutations within these cardiac genes do not appear to be the only cause of HCM in these breeds.
  • Evaluation of additional cardiac genes is warranted to identify additional molecular causes of this feline cardiac disease.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19566849.001).
  • [ISSN] 0891-6640
  • [Journal-full-title] Journal of veterinary internal medicine
  • [ISO-abbreviation] J. Vet. Intern. Med.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Muscle Proteins
  •  go-up   go-down


43. Yang ZJ, Ma DC, Wang W, Xu SL, Zhang YQ, Chen B, Zhou F, Zhu TB, Wang LS, Jia EZ, Zhang FM, Cao KJ, Xu ZQ, Ma WZ: Neovascularization and cardiomyocytes regeneration in acute myocardial infarction after bone marrow stromal cell transplantation: comparison of infarct-relative and noninfarct-relative arterial approaches in swine. Clin Chim Acta; 2007 Jun;381(2):114-8
MedlinePlus Health Information. consumer health - Heart Attack.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This alternative approach may have potential application in clinical practice.
  • The donor cell localization and differentiation were identified by immunohistochemical staining for BrdU and beta-myosin heavy chain (beta-MHC) and angiogenesis was assessed by immunohistochemical staining for alpha-smooth muscle actin (alpha-SMA) and Factor VIII.
  • [MeSH-minor] Acute Disease. Animals. Cell Separation. Coronary Circulation / physiology. Heart / physiopathology. Immunohistochemistry. Stromal Cells / transplantation. Swine

  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17400203.001).
  • [ISSN] 0009-8981
  • [Journal-full-title] Clinica chimica acta; international journal of clinical chemistry
  • [ISO-abbreviation] Clin. Chim. Acta
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  •  go-up   go-down


44. Yang G, Wang L, Zhu M, Xu D: Identification of non-Alzheimer's disease tauopathies-related proteins by proteomic analysis. Neurol Res; 2008 Jul;30(6):613-22

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of non-Alzheimer's disease tauopathies-related proteins by proteomic analysis.
  • METHOD: Two-dimensional gel electrophoresis (2DE) was applied to separate the total proteins of temporal lobe obtained at autopsy from four tauopathies cases and four aged subjects without clinical or pathologic involvement of nervous system.
  • The silver or Coomassie brilliant blue stained gels were analysed by 2-DE software Image Master 2D Elite.
  • RESULTS: Glyceraldehyde 3-phosphate dehydrogenase, uracil DNA glycosylase, human superoxide dismutase, isocitrate dehydrogenase subunit, synaptotagmin I, thioredoxin peroxidase 1, glial fibrillary acidic protein, P25 alpha, enoyl coenzyme A hydratase short chain 1, pyridoxine-5'-phosphate oxidase, Mn-superoxide dismutase and alpha enolase were significantly upregulated in tauopathies brains, whereas antioxidant protein 2, ferritin heavy chain, glutamate dehydrogenase precursor, peptidyl-prolyl cis-trans isomerase A, serum albumin precursor and dihydropyrimidinase-related protein 2 were lowly expressed in tauopathies brains.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18647502.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proteins
  •  go-up   go-down


45. Plager DA, Leontovich AA, Henke SA, Davis MD, McEvoy MT, Sciallis GF 2nd, Pittelkow MR: Early cutaneous gene transcription changes in adult atopic dermatitis and potential clinical implications. Exp Dermatol; 2007 Jan;16(1):28-36
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] Early cutaneous gene transcription changes in adult atopic dermatitis and potential clinical implications.
  • Therefore, we used high-density oligonucleotide arrays to identify cutaneous gene transcription changes associated with early AD inflammation as potential disease control targets.
  • Differential transcription occurring early in AD skin was indicated for (i) individual genes such as C-C chemokine ligand (CCL)18, CCL13, and interferon-alpha2 (IFNalpha2), (ii) genes associated with peroxisome proliferator-activated receptor (PPAR)alpha- and PPARgamma-regulated transcription, and possibly for (iii) immunoglobulin J-chain and heavy chain isotype transcripts.
  • These data suggest that local changes in immunoglobulin-associated transcription may favour IgE over secretory immunoglobulin (multimeric IgM and IgA) expression in AD skin.
  • [MeSH-minor] Adult. Biopsy. Case-Control Studies. Chemokines, CC / genetics. Chemokines, CC / metabolism. Female. Gene Expression Regulation. Humans. Immunoglobulin E / genetics. Immunoglobulin E / metabolism. Interferon-alpha / genetics. Interferon-alpha / metabolism. Male. Monocyte Chemoattractant Proteins / genetics. Monocyte Chemoattractant Proteins / metabolism. Oligonucleotide Array Sequence Analysis. PPAR alpha / genetics. PPAR alpha / metabolism. PPAR gamma / genetics. PPAR gamma / metabolism

  • Genetic Alliance. consumer health - Eczema.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17181634.001).
  • [ISSN] 0906-6705
  • [Journal-full-title] Experimental dermatology
  • [ISO-abbreviation] Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / CCL13 protein, human; 0 / CCL18 protein, human; 0 / Chemokines, CC; 0 / Interferon-alpha; 0 / Monocyte Chemoattractant Proteins; 0 / PPAR alpha; 0 / PPAR gamma; 37341-29-0 / Immunoglobulin E
  •  go-up   go-down


46. Buse C, Altmann F, Amann B, Hauck SM, Poulsen Nautrup C, Ueffing M, Stangassinger M, Deeg CA: Discovering novel targets for autoantibodies in dilated cardiomyopathy. Electrophoresis; 2008 Mar;29(6):1325-32
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Since DCM is a fatal disorder with rapid aggravation and is the leading cause of heart transplantation, further insights into disease pathogenesis are needed.
  • Recent studies have separated the pathogenic capacity of autoantibodies and initial clinical trials removing such autoantibodies via immunoadsorption have been promising.
  • With this method, we detected five potentially DCM-related autoantigens which were identified by MS as being: myosin heavy chain cardiac muscle alpha isoform, alpha cardiac actin, mitochondrial aconitate hydratase, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and brain glycogen phosphorylase (GPBB).
  • The recovery of two known DCM autoantigens (myosin heavy chain and alpha cardiac actin) and the discovery of three novel autoantigens (mitochondrial aconitate hydratase, GADPH, and GPBB) underscore the efficacy of this experimental method and the significance of the spontaneous canine DCM model.
  • [MeSH-major] Autoantibodies / immunology. Autoantigens / analysis. Cardiomyopathy, Dilated / immunology. Cardiomyopathy, Dilated / veterinary. Dog Diseases / immunology
  • [MeSH-minor] Aconitate Hydratase / immunology. Actins / immunology. Animals. Blotting, Western / methods. Dogs. Electrophoresis, Gel, Two-Dimensional / methods. Glyceraldehyde-3-Phosphate Dehydrogenases / immunology. Glycogen Phosphorylase, Brain Form / immunology. Ventricular Myosins / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18288668.001).
  • [ISSN] 0173-0835
  • [Journal-full-title] Electrophoresis
  • [ISO-abbreviation] Electrophoresis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Actins; 0 / Autoantibodies; 0 / Autoantigens; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases; EC 2.4.1.- / Glycogen Phosphorylase, Brain Form; EC 3.6.1.- / Ventricular Myosins; EC 4.2.1.3 / Aconitate Hydratase
  •  go-up   go-down


47. Murdaca G, Contini P, Setti M, Cagnati P, Villa R, Lantieri F, Indiveri F, Puppo F: Behavior of serum human major histocompatibility complex class I antigen levels in human immunodeficiency virus-infected patients during antiretroviral therapy: correlation with clinical outcome. Hum Immunol; 2007 Nov;68(11):894-900
HIV InSite. treatment guidelines - Palliative Care of Patients with HIV .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Behavior of serum human major histocompatibility complex class I antigen levels in human immunodeficiency virus-infected patients during antiretroviral therapy: correlation with clinical outcome.
  • Human major histocompatibility complex class I antigens (HLA-A, -B, and -C) are heterodimeric molecules composed of a alpha heavy chain noncovalently associated with an invariant protein known as beta(2)-microglobulin.
  • The introduction of highly active antiretroviral therapy (HAART) modified the clinical course of the disease and decreased the acquired immunodeficiency syndrome-related morbidity and mortality.
  • [MeSH-minor] Adult. CD4 Lymphocyte Count. Female. HIV / isolation & purification. Humans. Male. Middle Aged. RNA, Viral / blood. Receptors, Tumor Necrosis Factor, Type II / blood. Treatment Outcome. Viral Load. beta 2-Microglobulin / blood

  • MedlinePlus Health Information. consumer health - HIV/AIDS.
  • MedlinePlus Health Information. consumer health - HIV/AIDS in Women.
  • MedlinePlus Health Information. consumer health - HIV/AIDS Medicines.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18082568.001).
  • [ISSN] 0198-8859
  • [Journal-full-title] Human immunology
  • [ISO-abbreviation] Hum. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 0 / RNA, Viral; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / beta 2-Microglobulin
  •  go-up   go-down


48. Satoh M, Minami Y, Takahashi Y, Tabuchi T, Nakamura M: Expression of microRNA-208 is associated with adverse clinical outcomes in human dilated cardiomyopathy. J Card Fail; 2010 May;16(5):404-10
Genetic Alliance. consumer health - Dilated Cardiomyopathy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of microRNA-208 is associated with adverse clinical outcomes in human dilated cardiomyopathy.
  • BACKGROUND: Recently, microRNA-208 (miR-208) encoded by the alpha-myosin heavy chain (MHC) gene, has been shown to be involved in pathological cardiac growth, fibrosis, and up-regulation of beta-MHC expression.
  • The aim of this study was to determine whether miR-208, miR-208b, and miR-499 are expressed with MHC mRNA in human dilated cardiomyopathy (DCM), and whether these levels are related to left ventricular (LV) function and to clinical outcomes.
  • Levels of alpha-MHC mRNA were lower in patients with DCM than in controls, whereas beta-MHC mRNA levels were higher in patients with DCM compared with controls.
  • After a mean follow-up of 517 days, an increase in miR-208 levels was shown to be a strong predictor of clinical outcomes (RR 3.4, 95% CI 1.1-11.2).
  • CONCLUSIONS: This study suggests that myocardial expression of miR-208 is associated with MHC mRNA expression and with poor clinical outcomes in patients with DCM.
  • [MeSH-major] Cardiomyopathy, Dilated / genetics. MicroRNAs / genetics. Myosin Heavy Chains / genetics. Treatment Outcome
  • [MeSH-minor] Case-Control Studies. Collagen / biosynthesis. Collagen / genetics. Confidence Intervals. Disease Progression. Female. Humans. Japan. Logistic Models. Male. Middle Aged. Multivariate Analysis. Prognosis. Risk. Risk Factors. Statistics as Topic. Stroke Volume. Ventricular Function, Left. Ventricular Myosins / genetics

  • Genetic Alliance. consumer health - Cardiomyopathy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20447577.001).
  • [ISSN] 1532-8414
  • [Journal-full-title] Journal of cardiac failure
  • [ISO-abbreviation] J. Card. Fail.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MIRN499 microRNA, human; 0 / MicroRNAs; 9007-34-5 / Collagen; EC 3.6.1.- / Ventricular Myosins; EC 3.6.4.1 / Myosin Heavy Chains
  •  go-up   go-down


49. Kaderi MA, Murray F, Jansson M, Merup M, Karlsson K, Roos G, Aleskog A, Tobin G: The GNAS1 T393C polymorphism and lack of clinical prognostic value in chronic lymphocytic leukemia. Leuk Res; 2008 Jun;32(6):984-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The GNAS1 T393C polymorphism and lack of clinical prognostic value in chronic lymphocytic leukemia.
  • Chronic lymphocytic leukemia (CLL) is a clinically heterogeneous disease with no known single predisposing genetic factor shown in all cases.
  • Recently, a single nucleotide polymorphism (SNP) T393C in the GNAS1 gene has been reported to have a clinical impact on CLL progression and overall survival.
  • In order to further investigate the T393C SNP in CLL, we have genotyped 279 CLL cases and correlated the genotypes to clinical outcome and other known prognostic factors such as the immunoglobulin heavy chain variable (IGHV) gene mutation status and CD38 expression.
  • In summary, our data does not support the use of the T393C GNAS SNP as a clinical prognostic factor in CLL.
  • [MeSH-major] GTP-Binding Protein alpha Subunits, Gs / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Polymorphism, Single Nucleotide / genetics
  • [MeSH-minor] Aged. Antigens, CD38 / metabolism. Cohort Studies. DNA Primers. Disease Progression. Gene Expression Regulation, Leukemic. Genotype. Humans. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. Mutation / genetics. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18006055.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / RNA, Messenger; EC 3.2.2.5 / Antigens, CD38; EC 3.6.1.- / GNAS protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  •  go-up   go-down


50. Giusti L, Iacconi P, Ciregia F, Giannaccini G, Donatini GL, Basolo F, Miccoli P, Pinchera A, Lucacchini A: Fine-needle aspiration of thyroid nodules: proteomic analysis to identify cancer biomarkers. J Proteome Res; 2008 Sep;7(9):4079-88
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • At present, the clinical and pathological analysis used in the diagnosis of papillary thyroid cancer (PTC) are insufficient to discern tumor behavior, and new diagnostic and prognostic markers need to be identified.
  • These proteins included transthyretin precursor (TTR), ferritin light chain (FLC), proteasome activator complex subunit 1 and 2, alpha-1-antitrypsin precursor, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), lactate dehydrogenase chain B (LDH-B), apolipoprotein A1 precursor (Apo-A1), annexin A1, DJ-1 protein and cofilin-1.
  • These latter proteins (ferritin heavy chain (FHC), peroxiredoxin 1 (PRX1) and 6-phosphogluconate dehydrogenase (6-PDGH)) correspond to stress response proteins and, until now, had not been described in thyroid tumors.
  • These findings illustrate the potential use of FNA proteomics to identify protein changes associated with thyroid cancer and to advance potential protein biomarkers in the diagnostic classification of the disease.


51. Wirz W, Antoine M, Tag CG, Gressner AM, Korff T, Hellerbrand C, Kiefer P: Hepatic stellate cells display a functional vascular smooth muscle cell phenotype in a three-dimensional co-culture model with endothelial cells. Differentiation; 2008 Sep;76(7):784-94
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hepatic stellate cells (HSCs) are pericytes of liver sinusoidal endothelial cells (LSECs) and activation of HSC into a myofibroblast-like phenotype (called transdifferentiation) is involved in several hepatic disease processes including neovascularization during liver metastasis, chronic and acute liver injury.
  • While early smooth muscle cell (SMC) differentiation markers including SM alpha-actin and SM22alpha are expressed in a variety of non-SMC, expression of late-stage markers is far more restricted.
  • Here, we found that in addition to early SMC markers, activated rat HSC express a large panel of characteristic late vascular SMC markers including SM myosin heavy chain, h1-calponin and h-caldesmon.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18177423.001).
  • [ISSN] 1432-0436
  • [Journal-full-title] Differentiation; research in biological diversity
  • [ISO-abbreviation] Differentiation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Recombinant Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
  •  go-up   go-down


52. Kido M, Du L, Sullivan CC, Li X, Deutsch R, Jamieson SW, Thistlethwaite PA: Hypoxia-inducible factor 1-alpha reduces infarction and attenuates progression of cardiac dysfunction after myocardial infarction in the mouse. J Am Coll Cardiol; 2005 Dec 6;46(11):2116-24
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] Hypoxia-inducible factor 1-alpha reduces infarction and attenuates progression of cardiac dysfunction after myocardial infarction in the mouse.
  • OBJECTIVES: The aim of this research was to test whether constitutive expression of hypoxia-inducible factor 1-alpha (HIF-1alpha) influences infarction size and cardiac performance after myocardial infarction.
  • BACKGROUND: A major question in clinical medicine is whether infarction size and border zone remodeling of the heart can be influenced by the overexpression of specific genes in the peri-infarction region.
  • Transgenic mice containing the HIF-1alpha gene under the control of the alpha-myosin heavy chain promoter were constructed.
  • [MeSH-minor] Animals. Blotting, Northern. Blotting, Western. Disease Progression. Immunohistochemistry. Male. Mice. Mice, Transgenic. Neovascularization, Physiologic / physiology. Nitric Oxide Synthase Type II / metabolism. Transcription, Genetic / physiology. Vascular Endothelial Growth Factor A / metabolism. Ventricular Function, Left. Ventricular Remodeling / physiology

  • MedlinePlus Health Information. consumer health - Heart Attack.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16325051.001).
  • [ISSN] 1558-3597
  • [Journal-full-title] Journal of the American College of Cardiology
  • [ISO-abbreviation] J. Am. Coll. Cardiol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR00827; United States / NHLBI NIH HHS / HL / R01 HL70852
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1; 0 / Vascular Endothelial Growth Factor A; EC 1.14.13.39 / Nitric Oxide Synthase Type II
  •  go-up   go-down


53. Landolsi A, Chabchoub I, Limem S, Gharbi O, Chaafai R, Hochlef M, Fatma LB, Trimech M, Krifa A, Ajmi S, Mokni M, Hadj Hmida MB, Ahmed SB: [Primary digestive tract lymphoma in central region of Tunisia: anatomoclinical study and therapeutic results about 153 cases]. Bull Cancer; 2010 Apr;97(4):435-43

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Primary digestive tract lymphoma in central region of Tunisia: anatomoclinical study and therapeutic results about 153 cases].
  • [Transliterated title] Les lymphomes primitifs du tube digestif (LPTD) dans le centre tunisien: étude anatomoclinique et résultats thérapeutiques à propos de 153 cas.
  • Primary gastro-intestinal lymphoma (PGIL) is the most common type of extra-nodal non Hodgkin's lymphoma.
  • Their clinical and histological presentations are heterogeneous depending on the site of the lesion.
  • In our country epidemiology of the disease is unknown with IPSID being the most frequent type.
  • We report anatomo-clinical features and prognostic factors of PGIL and compare intestinal to gastric forms in our region.
  • Tumor sites were gastric (67%), intestinal (26%) and gastrointestinal (7%).
  • Abdominal pain (87%) followed by vomiting and diarrhoea (37 and 15%) were the most common symptoms.
  • Performance status (PS) < 2 was seen in 80% of patients, high grade lymphoma in 70.5% of cases and B phenotype was noted in 85%.
  • MALT lymphoma accounts for 50% of cases, and IPSID for only 5% of PGIL.
  • Only 46% of patients had surgery (14 for surgical complication, 6 for residual tumor after chemotherapy and 22 to have histological diagnosis).
  • In high grade lymphoma patients favorable prognostic factors for OS included young age < or = 60 years, PS < 2, normal serum LDH, hemoglobin > 12 g/dL, B phenotype, localised stage (IE-IIE1), anthracycline-based chemotherapy regimen, achieving complete or partial response to induction chemotherapy and no relapse.
  • In low-grade lymphoma patients, none of these factors had a significant correlation with OS: age < or = 60 years, PS < 2, stage (IE-IIE1), response to induction chemotherapy, relapse.
  • Compared to gastric lymphomas, intestinal cases occurred at a younger age, frequently with diarrhoea, weight loss, and occlusion.
  • We conclude that stomach is the main site of PGIL in our region, intestinal lymphoma is less frequent and IPSID has become rare.
  • [MeSH-major] Gastrointestinal Neoplasms. Lymphoma, Non-Hodgkin
  • [MeSH-minor] Abdominal Pain / etiology. Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Diarrhea / etiology. Female. Humans. Male. Middle Aged. Prognosis. Retrospective Studies. Tunisia. Vomiting / etiology. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20395189.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


54. Smith SC, Smith EC, Gilman ML, Anderson JL, Taylor RL Jr: Differentially expressed soluble proteins in aortic cells from atherosclerosis-susceptible and resistant pigeons. Poult Sci; 2008 Jul;87(7):1328-34
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Some of the annotated proteins (such as smooth muscle myosin phosphatase, myosin heavy chain, fatty acid-binding protein, ribophorin, heat shock protein, and tumor necrosis factor alpha-inducing factor) corresponded to the current hypotheses to explain atherogenesis.
  • In addition, the unique electrophoretic migration zones of proteins associated with susceptibility or resistance should prove useful as a diagnostic tool in clinical settings where species or phenotypes, or both, susceptible or resistant to atherosclerosis can be identified.
  • [MeSH-major] Aorta / cytology. Atherosclerosis / veterinary. Columbidae / genetics. Gene Expression Profiling. Poultry Diseases / genetics
  • [MeSH-minor] Animals. Cells, Cultured. Genetic Predisposition to Disease. Lipoproteins / genetics. Lipoproteins / metabolism

  • MedlinePlus Health Information. consumer health - Atherosclerosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18577612.001).
  • [ISSN] 0032-5791
  • [Journal-full-title] Poultry science
  • [ISO-abbreviation] Poult. Sci.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / 1R15HL072786-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipoproteins
  •  go-up   go-down


55. Krebs P, Kurrer MO, Kremer M, De Giuli R, Sonderegger I, Henke A, Maier R, Ludewig B: Molecular mapping of autoimmune B cell responses in experimental myocarditis. J Autoimmun; 2007 Jun;28(4):224-33
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.
  • Screening of a heart cDNA library with sera of cardiac myosin heavy chain alpha (myhcalpha) peptide-immunized BALB/c mice revealed a strong focusing of the B cell response on the myhcalpha protein.
  • [MeSH-major] Autoantibodies / immunology. Autoimmune Diseases / immunology. B-Lymphocytes / immunology. Myocarditis / immunology. Myocardium / immunology. Myosin Heavy Chains / immunology

  • Genetic Alliance. consumer health - Myocarditis.
  • Genetic Alliance. consumer health - Autoimmune Myocarditis.
  • MedlinePlus Health Information. consumer health - Autoimmune Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17336498.001).
  • [ISSN] 0896-8411
  • [Journal-full-title] Journal of autoimmunity
  • [ISO-abbreviation] J. Autoimmun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Epitopes, B-Lymphocyte; EC 3.6.4.1 / Myosin Heavy Chains
  •  go-up   go-down


56. Mattioli M, Agnelli L, Fabris S, Baldini L, Morabito F, Bicciato S, Verdelli D, Intini D, Nobili L, Cro L, Pruneri G, Callea V, Stelitano C, Maiolo AT, Lombardi L, Neri A: Gene expression profiling of plasma cell dyscrasias reveals molecular patterns associated with distinct IGH translocations in multiple myeloma. Oncogene; 2005 Apr 7;24(15):2461-73
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.
  • Multiple myeloma (MM) is the most common form of plasma cell dyscrasia, characterized by a marked heterogeneity of genetic lesions and clinical course.
  • To provide insights into the molecular characterization of plasma cell dyscrasias and to investigate the contribution of specific genetic lesions to the biological and clinical heterogeneity of MM, we analysed the gene expression profiles of plasma cells isolated from seven MGUS, 39 MM and six PCL patients by means of DNA microarrays.
  • The clustering of MM patients was mainly driven by the presence of the most recurrent translocations involving the immunoglobulin heavy-chain locus.
  • The peculiar finding in patients with the t(11;14) was the downregulation of the alpha-subunit of the IL-6 receptor.
  • In addition, we identified a set of cancer germline antigens specifically expressed in a subgroup of MM patients characterized by an aggressive clinical evolution, a finding that could have implications for patient classification and immunotherapy.
  • [MeSH-major] Gene Expression Profiling. Genetic Predisposition to Disease. Leukemia, Plasma Cell / genetics. Leukemia, Plasma Cell / physiopathology. Multiple Myeloma / genetics. Multiple Myeloma / physiopathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis. Cyclin D2. Cyclins / biosynthesis. DNA, Neoplasm / analysis. Down-Regulation. Female. Humans. Immunoglobulin Heavy Chains. Male. Middle Aged. Prognosis. Receptors, Interleukin-6 / biosynthesis. Translocation, Genetic. Up-Regulation

  • Genetic Alliance. consumer health - Multiple myeloma.
  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15735737.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / DNA, Neoplasm; 0 / Immunoglobulin Heavy Chains; 0 / Receptors, Interleukin-6
  •  go-up   go-down


57. Iemitsu M, Shimojo N, Maeda S, Irukayama-Tomobe Y, Sakai S, Ohkubo T, Tanaka Y, Miyauchi T: The benefit of medium-chain triglyceride therapy on the cardiac function of SHRs is associated with a reversal of metabolic and signaling alterations. Am J Physiol Heart Circ Physiol; 2008 Jul;295(1):H136-44
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] The benefit of medium-chain triglyceride therapy on the cardiac function of SHRs is associated with a reversal of metabolic and signaling alterations.
  • The spontaneously hypertensive rat (SHR) is a model of cardiomyopathy that displays a genetic defect in cardiac fatty acid (FA) translocase/CD36, a plasma membrane long-chain FA transporter.
  • Therapy with medium-chain FAs, which do not require CD36-facilitated transport, has been shown to improve cardiac function and hypertrophy in SHRs despite persistent hypertension.
  • The aim of this study was to document the impact of medium-chain triglyceride (MCT) therapy in SHRs on the expression level and activity of metabolic enzymes and signaling pathways.
  • Four-week-old male SHRs were administered MCT (SHR-MCT) or long-chain triglyceride (SHR-LCT) for 16 wk.
  • The SHR-MCT group displayed improved cardiac dysfunction [as assessed by left ventricular (LV) end-diastolic pressure and the positive and negative first derivatives of LV pressure/P value], a shift in the beta-myosin heavy chain (MHC)-to-alpha-MHC ratio, and cardiac hypertrophy compared with the SHR-LCT group without an effect on blood pressure.
  • Administration of MCT of SHRs reversed the LCT-induced reduction in the cardiac FA metabolic enzymatic activities of long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) and medium-chain acyl-CoA dehydrogenase (MCAD).
  • In the SHR-MCT group, the protein expression and transcriptional regulation of myocardial peroxisome proliferator-activated receptor-alpha, which regulates the transcription of LCHAD and MCAD genes, corresponded to the changes seen in those enzymatic activities.
  • [MeSH-minor] 3-Hydroxyacyl CoA Dehydrogenases / metabolism. Acyl-CoA Dehydrogenase / metabolism. Animals. Antigens, CD36 / metabolism. Blood Pressure / drug effects. Disease Models, Animal. JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors. JNK Mitogen-Activated Protein Kinases / metabolism. Long-Chain-3-Hydroxyacyl-CoA Dehydrogenase. Male. Myosin Heavy Chains / metabolism. PPAR alpha / metabolism. Phosphorylation. RNA, Messenger / metabolism. Rats. Rats, Inbred SHR. Rats, Inbred WKY. Time Factors. Transcription, Genetic. Ventricular Myosins / metabolism. Ventricular Pressure / drug effects

  • MedlinePlus Health Information. consumer health - High Blood Pressure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18456726.001).
  • [ISSN] 0363-6135
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD36; 0 / Bmyo protein, rat; 0 / Cd36 protein, rat; 0 / PPAR alpha; 0 / RNA, Messenger; 0 / Triglycerides; EC 1.1.1.- / 3-Hydroxyacyl CoA Dehydrogenases; EC 1.1.1.211 / Long-Chain-3-Hydroxyacyl-CoA Dehydrogenase; EC 1.3.8.7 / Acyl-CoA Dehydrogenase; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.6.1.- / Ventricular Myosins; EC 3.6.4.1 / Myosin Heavy Chains
  •  go-up   go-down


58. Zhou CQ, Yan JT, Fan Q, Li ZY, Cianflone K, Wang DW: [Throat infection, neck spinal disease, chest pain and cardiac response: a new clinical syndrome?]. Zhonghua Xin Xue Guan Bing Za Zhi; 2010 Feb;38(2):147-51
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] [Throat infection, neck spinal disease, chest pain and cardiac response: a new clinical syndrome?].
  • OBJECTIVE: To analyze the characteristics of a new clinical syndrome, including throat infection, neck spinal disease, chest pain and cardiac response.
  • Serum myocardial auto-antibodies against beta(1)-adrenoceptor, alpha-myosin heavy chain, M(2)-muscarinic receptor and adenine-nucleotide translocator were detected, inflammatory cytokines, high sensitivity C-reaction protein, serum antibodies against Coxsackie virus-B, cytomegalovirus, Mycoplasma pneumoniae and Chlamydia pneumoniae were determined and lymphocyte subclasses were assayed by flow cytometry.
  • TNF-alpha, IL-1 and IL-6 were significantly higher in patients than controls (P < 0.01).
  • CONCLUSIONS: These data led to identification of a persistent respiratory infection-related clinical syndrome, including persistent throat infection, neck spinal lesion, rib cartilage inflammation, symptoms of cardiac depression and dyspnea with or without anxiety.
  • [MeSH-major] Chest Pain. Heart Diseases. Neck Pain. Respiratory Tract Diseases / diagnosis. Spinal Diseases
  • [MeSH-minor] Adolescent. Adult. Aged. Anxiety / diagnosis. Case-Control Studies. Female. Humans. Inflammation. Male. Middle Aged. Syndrome. Young Adult


59. Khositseth S, Kanitsap N, Warnnissorn N, Thongboonkerd V: IgA nephropathy associated with Hodgkin's disease in children: a case report, literature review and urinary proteome analysis. Pediatr Nephrol; 2007 Apr;22(4):541-6
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] IgA nephropathy associated with Hodgkin's disease in children: a case report, literature review and urinary proteome analysis.
  • We report herein a rare case of IgAN associated with Hodgkin's disease in a 14-year-old boy.
  • Clinical manifestations and laboratory parameters were improved after treatment with CHOP chemotherapy and enalapril.
  • Quantitative intensity analysis and gel mapping revealed 14 altered proteins with reduced excretion levels during the treatment course, including albumin, albumin complexed with decanoic acid, alpha-1 antitrypsin, cadherin-11 precursor, collagen alpha 1 (VI) chain precursor, complement C1q tumor necrosis factor-related protein, Ig heavy chain, Ig light chain, kininogen, inter-alpha-trypsin inhibitor (alpha-1 microglobulin), inter-alpha-trypsin inhibitor heavy chain, leucine-rich alpha-2 glycoprotein, beta-2 microglobulin, and transferrin precursor.
  • [MeSH-major] Biomarkers / metabolism. Glomerulonephritis, IGA / complications. Hodgkin Disease / complications. Proteins / metabolism. Proteome / metabolism

  • MedlinePlus Health Information. consumer health - Hodgkin Disease.
  • 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 = 17143626.001).
  • [ISSN] 0931-041X
  • [Journal-full-title] Pediatric nephrology (Berlin, Germany)
  • [ISO-abbreviation] Pediatr. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Proteins; 0 / Proteome
  •  go-up   go-down


60. Quartuccio L, De Re V, Fabris M, Marzotto A, Franzolini N, Gasparotto D, Caggiari L, Ferraccioli G, Scott CA, De Vita S: Atypical lymphoproliferation progressing into B-cell lymphoma in rheumatoid arthritis treated with different biological agents: clinical course and molecular characterization. Haematologica; 2006 May;91(5):691-4
Hazardous Substances Data Bank. CYCLOSPORIN A .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical lymphoproliferation progressing into B-cell lymphoma in rheumatoid arthritis treated with different biological agents: clinical course and molecular characterization.
  • A patient with rheumatoid arthritis (RA) developed an atypical lymphoproliferative disorder (LPD) after methotrexate and cyclosporine A, which regressed after suspension of both drugs.
  • Anti-tumor necrosis factor a therapy was used when the arthritis relapsed, but an aggressive B-cell non Hodgkin's lymphoma developed.
  • A minor clone with significant sequence homology to B-cell lymphomas arising in Sjogren's syndrome and mixed cryoglobulinemia syndrome, given rise to the non-Hodgkin's lymphoma.
  • Treatment of rheumatoid arthritis associated with lymphoproliferation represents a clinical challenge, and common pathogenetic pathways to lymphoma may occur in different autoimmune diseases.
  • [MeSH-major] Antirheumatic Agents / therapeutic use. Arthritis, Rheumatoid / complications. Immunosuppressive Agents / therapeutic use. Lymphoma, Large B-Cell, Diffuse / etiology. Lymphoproliferative Disorders / complications
  • [MeSH-minor] Aged. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Autoimmune Diseases / complications. Cyclosporine / adverse effects. Cyclosporine / therapeutic use. DNA, Neoplasm / genetics. Disease Progression. Disease Susceptibility. Etanercept. Female. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Gene Rearrangement, B-Lymphocyte, Light Chain. Genes, Immunoglobulin. Humans. Immunocompromised Host. Immunoglobulin G / adverse effects. Immunoglobulin G / contraindications. Immunoglobulin G / therapeutic use. Methotrexate / adverse effects. Methotrexate / therapeutic use. Neoplasm Proteins / analysis. Neoplasm Proteins / genetics. Receptors, Tumor Necrosis Factor / therapeutic use. Rituximab. Tumor Necrosis Factor-alpha / antagonists & inhibitors

  • Genetic Alliance. consumer health - Arthritis.
  • Genetic Alliance. consumer health - Rheumatoid arthritis.
  • MedlinePlus Health Information. consumer health - Rheumatoid Arthritis.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. Etanercept .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16670074.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antirheumatic Agents; 0 / DNA, Neoplasm; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; 0 / Neoplasm Proteins; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; 4F4X42SYQ6 / Rituximab; 83HN0GTJ6D / Cyclosporine; OP401G7OJC / Etanercept; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


61. Toussirot E, Wendling D: [The immunogenetics of ankylosing spondylitis]. Rev Med Interne; 2006 Oct;27(10):762-71
MedlinePlus Health Information. consumer health - Ankylosing Spondylitis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Immunogénétique de la spondylarthrite ankylosante.
  • BACKGROUND: Ankylosing spondylitis (AS) is an inflammatory rheumatic disease with axial involvement but its physiopathology remains unexplained.
  • A genetic background in AS is suggested by familial cases, concordance rate in twins and transmission of the disease in siblings.
  • HLA-B27 is directly associated with the disease physiopathology as suggested by animal models of rats transgenic for human HLA-B27 and beta2 microglobulin.
  • This HLA molecule have original biological properties, in particular a slow heavy chain folding and the formation of heavy chain homodimers without light chain.
  • FUTURE PROSPECTS AND PROJECTS: Thus in AS, the inflammatory process and then the clinical consequences may be explained by the involvement of HLA-B27, a bacterial antigen presentation, an abnormal immune response and the contribution of innate immunity, T CD4+ but also T CD8+ cells.
  • The original molecular structures of HLA-B27 are certainly involved in this complex physiopathology, but their direct influence on the disease remains to be precised.

  • Genetic Alliance. consumer health - Ankylosing Spondylitis.
  • Genetic Alliance. consumer health - Spondylitis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16782239.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cytokines; 0 / HLA-B27 Antigen; 0 / Peptides; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 66
  •  go-up   go-down


62. Sulda ML, Abbott CA, Macardle PJ, Hall RK, Kuss BJ: Expression and prognostic assessment of dipeptidyl peptidase IV and related enzymes in B-cell chronic lymphocytic leukemia. Cancer Biol Ther; 2010 Jul 15;10(2):180-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This study also shows that DP8 mRNA expression is significantly upregulated in CLL compared to normal tonsil B-lymphocytes (p < 0.05) which may suggest biological importance in this disease.
  • DP expression could not be correlated with any molecular or clinical prognostic markers for CLL in this cohort including IgVH mutational status, CD38, ZAP-70 or CD49d expression (n = 58).
  • However, the constitutive expression of the DPIV-like enzymes in CLL and their emergence as potent immune regulators makes them candidate therapeutic targets in this disease.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Dipeptidases / genetics. Dipeptidases / metabolism. Dipeptidyl-Peptidases and Tripeptidyl-Peptidases / genetics. Dipeptidyl-Peptidases and Tripeptidyl-Peptidases / metabolism. Female. Gelatinases / genetics. Gelatinases / metabolism. Gene Expression Profiling. Genes, Immunoglobulin Heavy Chain / genetics. Humans. Male. Membrane Proteins / genetics. Membrane Proteins / metabolism. Middle Aged. Mitochondrial Proteins / genetics. Mitochondrial Proteins / metabolism. Mutation. Prognosis. Serine Endopeptidases / genetics. Serine Endopeptidases / metabolism. Up-Regulation

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20534982.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / Mitochondrial Proteins; 0 / RNA, Messenger; EC 2.4.21.25 / PREP protein, human; EC 3.4.13.- / Dipeptidases; EC 3.4.14.- / DPP9 protein, human; EC 3.4.14.- / Dipeptidyl-Peptidases and Tripeptidyl-Peptidases; EC 3.4.14.2 / dipeptidyl peptidase II; EC 3.4.14.5 / DPP8 protein, human; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
  •  go-up   go-down


63. Carrier L, Schlossarek S, Willis MS, Eschenhagen T: The ubiquitin-proteasome system and nonsense-mediated mRNA decay in hypertrophic cardiomyopathy. Cardiovasc Res; 2010 Jan 15;85(2):330-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Over the last 20 years, the genetic basis of the disease has been largely unravelled.
  • HCM is considered as a sarcomeropathy involving mutations in sarcomeric proteins, most often beta-myosin heavy chain and cardiac myosin-binding protein C.
  • This review discusses clinical and genetic aspects of HCM and the role of NMD and UPS in the regulation of mutant proteins, evidence for impairment of UPS as a pathogenic factor, as well as potential therapies for HCM.
  • [MeSH-minor] Animals. Cardiomegaly / metabolism. Carrier Proteins / metabolism. Heart Failure / metabolism. Humans. Mutation. Myosin Heavy Chains / genetics. alpha-Crystallin B Chain / genetics

  • Genetic Alliance. consumer health - Cardiomyopathy.
  • Genetic Alliance. consumer health - Hypertrophic Cardiomyopathy.
  • COS Scholar Universe. author profiles.
  • 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
  • [Cites] Circ Res. 1999 Oct 29;85(9):841-7 [10532952.001]
  • [Cites] J Mol Biol. 1999 Nov 26;294(2):443-56 [10610770.001]
  • [Cites] Circulation. 2000 Mar 28;101(12):1396-402 [10736283.001]
  • [Cites] N Engl J Med. 2000 Jun 15;342(24):1778-85 [10853000.001]
  • [Cites] Circ Res. 2001 Jul 6;89(1):84-91 [11440982.001]
  • [Cites] Hypertension. 2001 Dec 1;38(6):1278-81 [11751703.001]
  • [Cites] JAMA. 2002 Mar 13;287(10):1308-20 [11886323.001]
  • [Cites] J Med Genet. 2002 Oct;39(10):741-6 [12362031.001]
  • [Cites] Swiss Med Wkly. 2002 Jul 27;132(29-30):401-7 [12428185.001]
  • [Cites] Proteomics. 2003 Feb;3(2):208-16 [12601813.001]
  • [Cites] Circulation. 2003 May 6;107(17):2227-32 [12707239.001]
  • [Cites] Acta Myol. 2003 May;22(1):15-21 [12966700.001]
  • [Cites] Am J Pathol. 2003 Oct;163(4):1663-75 [14507673.001]
  • [Cites] Cardiovasc Res. 2003 Nov 1;60(2):388-96 [14613868.001]
  • [Cites] J Mol Cell Cardiol. 2004 Mar;36(3):355-62 [15010274.001]
  • [Cites] Lancet. 2004 Jun 5;363(9424):1881-91 [15183628.001]
  • [Cites] Cardiovasc Res. 2004 Aug 1;63(2):293-304 [15249187.001]
  • [Cites] Curr Opin Pulm Med. 2004 Nov;10(6):547-52 [15510065.001]
  • [Cites] FEBS Lett. 1988 Apr 25;231(2):421-5 [3360147.001]
  • [Cites] J Clin Invest. 1993 Dec;92(6):2807-13 [8254035.001]
  • [Cites] Circulation. 1995 Aug 15;92(4):785-9 [7641357.001]
  • [Cites] Circulation. 1996 Mar 1;93(5):841-2 [8598070.001]
  • [Cites] Circ Res. 1997 Mar;80(3):427-34 [9048664.001]
  • [Cites] J Muscle Res Cell Motil. 1997 Jun;18(3):275-83 [9172070.001]
  • [Cites] Genet Couns. 1997;8(2):107-14 [9219008.001]
  • [Cites] J Clin Invest. 1997 Jul 15;100(2):475-82 [9218526.001]
  • [Cites] Circulation. 1997 Jul 1;96(1):214-9 [9236436.001]
  • [Cites] Circ Res. 1998 Jan 9-23;82(1):106-15 [9440709.001]
  • [Cites] Circ Res. 1998 Jan 9-23;82(1):130-3 [9440712.001]
  • [Cites] Eur Heart J. 1998 Jan;19(1):139-45 [9503187.001]
  • [Cites] J Med Genet. 1998 Mar;35(3):205-10 [9541104.001]
  • [Cites] N Engl J Med. 1998 Apr 30;338(18):1248-57 [9562578.001]
  • [Cites] Nat Genet. 1998 Sep;20(1):92-5 [9731540.001]
  • [Cites] Eur Heart J. 1998 Sep;19(9):1377-82 [9792264.001]
  • [Cites] Hypertension. 1998 Nov;32(5):825-30 [9822439.001]
  • [Cites] Antimicrob Agents Chemother. 1999 May;43(5):1003-12 [10223907.001]
  • [Cites] Br Heart J. 1958 Jan;20(1):1-8 [13499764.001]
  • [Cites] Pharmacogenomics. 2005 Jan;6(1):27-36 [15723603.001]
  • [Cites] Cardiovasc Res. 2005 Apr 1;66(1):33-44 [15769446.001]
  • [Cites] J Cell Sci. 2005 May 1;118(Pt 9):1773-6 [15860725.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13592-7 [16155124.001]
  • [Cites] J Am Coll Cardiol. 2005 Oct 18;46(8):1543-50 [16226182.001]
  • [Cites] Circ Res. 2005 Nov 11;97(10):1018-26 [16210548.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Feb 24;340(4):1125-33 [16403436.001]
  • [Cites] Cardiovasc Res. 2006 Feb 1;69(2):370-80 [16380103.001]
  • [Cites] Neurology. 2006 Jan 24;66(2 Suppl 1):S7-19 [16432150.001]
  • [Cites] FASEB J. 2006 Feb;20(2):362-4 [16371426.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Apr 7;342(2):361-4 [16483544.001]
  • [Cites] J Mol Cell Cardiol. 2006 Apr;40(4):451-4 [16481005.001]
  • [Cites] Cardiovasc Res. 2006 Jun 1;70(3):410-21 [16497285.001]
  • [Cites] BMC Cancer. 2006;6:129 [16689991.001]
  • [Cites] Mol Ther. 2006 Sep;14(3):351-60 [16807116.001]
  • [Cites] J Mol Cell Cardiol. 2006 Oct;41(4):669-79 [16928382.001]
  • [Cites] Trends Biochem Sci. 2006 Nov;31(11):639-46 [17010613.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Dec 29;351(4):1011-7 [17097067.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Feb;8(2):113-26 [17245413.001]
  • [Cites] J Mol Biol. 2007 Mar 16;367(1):36-41 [17254601.001]
  • [Cites] J Clin Pharmacol. 2007 Apr;47(4):430-44 [17389552.001]
  • [Cites] Arch Mal Coeur Vaiss. 2007 Mar;100(3):238-43 [17536430.001]
  • [Cites] Annu Rev Biochem. 2007;76:51-74 [17352659.001]
  • [Cites] Circulation. 2007 Jul 3;116(1):17-24 [17576861.001]
  • [Cites] Br J Haematol. 2007 Aug;138(3):396-7 [17561972.001]
  • [Cites] JAMA. 2007 Jul 25;298(4):405-12 [17652294.001]
  • [Cites] PLoS Genet. 2007 Jun;3(6):e109 [17604456.001]
  • [Cites] Circ Res. 2007 Oct 26;101(9):928-38 [17823372.001]
  • [Cites] Genomics. 2008 Jan;91(1):52-60 [18060737.001]
  • [Cites] Eur Heart J. 2008 Jan;29(2):270-6 [17916581.001]
  • [Cites] J Cardiovasc Electrophysiol. 2008 Jan;19(1):104-10 [17916152.001]
  • [Cites] Hypertension. 2008 Feb;51(2):302-8 [18086945.001]
  • [Cites] Cardiovasc Res. 2008 Feb 1;77(3):497-505 [18006445.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2008 Feb;294(2):H645-50 [18032525.001]
  • [Cites] J Mol Med (Berl). 2008 Mar;86(3):281-9 [17987279.001]
  • [Cites] Biophys J. 2008 Jul;95(2):720-8 [18375505.001]
  • [Cites] Cardiovasc Res. 2008 Aug 1;79(3):472-80 [18375498.001]
  • [Cites] Int J Hematol. 2008 Sep;88(2):219-22 [18633693.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2008 Oct;295(4):H1385-93 [18676687.001]
  • [Cites] Trends Genet. 2008 Nov;24(11):552-63 [18937996.001]
  • [Cites] J Mol Biol. 2008 Dec 26;384(4):896-907 [18929575.001]
  • [Cites] Biochim Biophys Acta. 2008 Dec;1782(12):749-63 [18634872.001]
  • [Cites] Cardiovasc Res. 2009 Feb 15;81(3):439-48 [18974044.001]
  • [Cites] Ernst Schering Found Symp Proc. 2008;(1):171-90 [19202599.001]
  • [Cites] J Clin Pathol. 2009 Mar;62(3):226-35 [18930982.001]
  • [Cites] Circulation. 2009 Mar 24;119(11):1473-83 [19273718.001]
  • [Cites] Clin Biochem. 2009 Jun;42(9):755-65 [19318019.001]
  • [Cites] Eur Heart J. 2009 Jul;30(13):1648-55 [19429631.001]
  • [Cites] Circ Res. 2009 Jul 31;105(3):239-48 [19590044.001]
  • [Cites] Cardiovasc Res. 2010 Jan 15;85(2):321-9 [19578073.001]
  • [Cites] Cardiovasc Res. 2010 Jan 15;85(2):357-66 [19850579.001]
  • [Cites] Mol Cell Biol. 1998 Sep;18(9):5272-83 [9710612.001]
  • (PMID = 19617224.001).
  • [ISSN] 1755-3245
  • [Journal-full-title] Cardiovascular research
  • [ISO-abbreviation] Cardiovasc. Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL104129
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CRYAB protein, human; 0 / Carrier Proteins; 0 / Ubiquitin; 0 / alpha-Crystallin B Chain; 0 / myosin-binding protein C; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 3.6.4.1 / Myosin Heavy Chains
  • [Number-of-references] 92
  • [Other-IDs] NLM/ PMC4023315
  •  go-up   go-down


64. Stirn Kranjc B, Smerdu V, Erzen I: Histochemical and immunohistochemical profile of human and rat ocular medial rectus muscles. Graefes Arch Clin Exp Ophthalmol; 2009 Nov;247(11):1505-15
SciCrunch. The Antibody Registry: Reagent: Antibodies .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To reveal myosin heavy chain (MyHC) isoforms, specific monoclonal antibodies against MyHC-1/beta- slow, alpha-cardiac (-alpha), -2a, -2x, -2b, -extraocular (eom), -embryonic (-emb) and -neonatal (-neo) were applied.
  • In the orbital layer most fibers were highly oxidative and expressed fast MyHC isoforms, whereas slow and oxidative fibers expressed MyHC-1 and -alpha, some of them also MyHC-2a, -2x, -eom, very rarely -emb, and -neo.
  • The slow medium-sized fibers with mATPase activity stable at pH 4.4 expressed mostly MyHC-1 and -alpha in rat, while in humans they co-expressed MyHC-1 with -2b, -2x, -eom, and -neo.
  • In both species, the fast fibers showed variable mATPase activity after preincubation at pH 9.4, and co-expressed various combinations of MyHC-2b, -2x, -2a and -eom but not -emb and -neo.
  • CONCLUSIONS: Rat MR represent a good model that can be applied to study human MR in experiment or disease, however certain differences are to be expected due to specific oculomotor demands in humans.
  • [MeSH-minor] Adenosine Triphosphatases / metabolism. Adult. Animals. Female. Glycerol-3-Phosphate Dehydrogenase (NAD+) / metabolism. Humans. Immunoenzyme Techniques. In Situ Hybridization. Male. Middle Aged. Models, Biological. Myosin Heavy Chains / metabolism. Protein Isoforms / metabolism. Rats. Rats, Wistar. Succinate Dehydrogenase / metabolism. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Sep;45(9):3067-72 [15326122.001]
  • [Cites] Exp Neurol. 1970 Aug;28(2):365-7 [4248172.001]
  • [Cites] Invest Ophthalmol. 1972 Dec;11(12):956-69 [4264336.001]
  • [Cites] Arch Ophthalmol. 1978 Jun;96(6):1067-72 [655944.001]
  • [Cites] J Morphol. 1982 Nov;174(2):237-50 [7175945.001]
  • [Cites] J Embryol Exp Morphol. 1982 Oct;71:171-91 [7153694.001]
  • [Cites] Histochemistry. 1984;80(6):535-8 [6236177.001]
  • [Cites] Histochemistry. 1984;80(5):429-33 [6237078.001]
  • [Cites] J Neurol Sci. 1984 Oct;66(1):107-15 [6240526.001]
  • [Cites] J Cell Biol. 1985 Aug;101(2):618-29 [3894379.001]
  • [Cites] FEBS Lett. 1988 Aug 1;235(1-2):153-5 [3402594.001]
  • [Cites] J Muscle Res Cell Motil. 1990 Feb;11(1):25-40 [2141031.001]
  • [Cites] Bull Soc Belge Ophtalmol. 1989;237:303-19 [2535013.001]
  • [Cites] Rev Physiol Biochem Pharmacol. 1990;116:1-76 [2149884.001]
  • [Cites] Acta Pathol Jpn. 1990 Nov;40(11):808-14 [2077814.001]
  • [Cites] Histochemistry. 1991;95(6):579-83 [1856112.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1992 Mar;33(3):657-70 [1544790.001]
  • [Cites] Development. 1992 Jan;114(1):1-15 [1576952.001]
  • [Cites] Histochemistry. 1993 Aug;100(2):149-53 [8244766.001]
  • [Cites] FEBS Lett. 1993 Dec 6;335(2):243-5 [8253205.001]
  • [Cites] Am J Physiol. 1994 Dec;267(6 Pt 1):C1723-8 [7545970.001]
  • [Cites] Surv Ophthalmol. 1995 May-Jun;39(6):451-84 [7660301.001]
  • [Cites] J Muscle Res Cell Motil. 1996 Jun;17(3):297-312 [8814550.001]
  • [Cites] J Appl Physiol (1985). 1998 Aug;85(2):584-92 [9688736.001]
  • [Cites] J Histochem Cytochem. 1955 May;3(3):170-95 [14381606.001]
  • [Cites] Eur J Histochem. 2004 Oct-Dec;48(4):357-66 [15718201.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Aug;46(8):2790-9 [16043852.001]
  • [Cites] Cells Tissues Organs. 2005;180(2):106-16 [16113539.001]
  • [Cites] J Exp Biol. 2005 Nov;208(Pt 22):4243-53 [16272247.001]
  • [Cites] Mol Vis. 2006;12:243-50 [16604057.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Oct;47(10):4188-93 [17003405.001]
  • [Cites] Eur J Histochem. 2008 Jul-Sep;52(3):179-90 [18840559.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2009 Jan;50(1):157-67 [18676637.001]
  • [Cites] Physiol Genomics. 2009 Mar 3;37(1):35-42 [19116248.001]
  • [Cites] J Muscle Res Cell Motil. 1999 Nov;20(8):771-83 [10730580.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Apr;41(5):980-90 [10752931.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Jun;41(7):1608-16 [10845576.001]
  • [Cites] Biochem Biophys Res Commun. 2000 May 27;272(1):303-8 [10872844.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Oct;41(11):3391-8 [11006229.001]
  • [Cites] J Muscle Res Cell Motil. 2000;21(8):753-61 [11392557.001]
  • [Cites] Arch Oral Biol. 2001 Nov;46(11):1039-50 [11543711.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2001 Dec;42(13):3158-64 [11726617.001]
  • [Cites] J Muscle Res Cell Motil. 2001;22(8):647-55 [12222825.001]
  • [Cites] J Exp Biol. 2002 Oct;205(Pt 20):3133-42 [12235193.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Apr;44(4):1419-25 [12657575.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Jun;44(6):2450-6 [12766042.001]
  • [Cites] J Biol Chem. 2003 Sep 26;278(39):37132-8 [12851393.001]
  • [Cites] Physiol Genomics. 2004 Jul 8;18(2):184-95 [15138310.001]
  • (PMID = 19609551.001).
  • [ISSN] 1435-702X
  • [Journal-full-title] Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv für klinische und experimentelle Ophthalmologie
  • [ISO-abbreviation] Graefes Arch. Clin. Exp. Ophthalmol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Protein Isoforms; EC 1.1.1.8 / Glycerol-3-Phosphate Dehydrogenase (NAD+); EC 1.3.99.1 / Succinate Dehydrogenase; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.4.1 / Myosin Heavy Chains
  • [Other-IDs] NLM/ PMC2758108
  •  go-up   go-down


65. Holaska JM, Wilson KL: An emerin "proteome": purification of distinct emerin-containing complexes from HeLa cells suggests molecular basis for diverse roles including gene regulation, mRNA splicing, signaling, mechanosensing, and nuclear architecture. Biochemistry; 2007 Jul 31;46(30):8897-908
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • These proteins were identified by mass spectrometry as nuclear alphaII-spectrin, nonmuscle myosin heavy chain alpha, Lmo7 (a predicted transcription regulator; reported separately), nuclear myosin I, beta-actin (reported separately), calponin 3, and SIKE.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] EMBO Rep. 2005 May;6(5):445-51 [15832170.001]
  • [Cites] Biochem Cell Biol. 2005 Aug;83(4):405-17 [16094444.001]
  • [Cites] J Cell Biol. 2005 Aug 29;170(5):781-91 [16115958.001]
  • [Cites] J Cell Sci. 2005 Sep 1;118(Pt 17):4017-25 [16129885.001]
  • [Cites] J Proteome Res. 2005 Sep-Oct;4(5):1661-71 [16212419.001]
  • [Cites] J Biol Chem. 2005 Dec 2;280(48):39925-33 [16204256.001]
  • [Cites] Development. 2005 Dec;132(24):5565-75 [16280346.001]
  • [Cites] Anticancer Drugs. 2006 Jan;17(1):13-20 [16317285.001]
  • [Cites] J Biol Chem. 1999 Nov 12;274(46):32904-8 [10551855.001]
  • [Cites] Gene. 1999 Oct 18;239(1):15-27 [10571030.001]
  • [Cites] Hum Mol Genet. 2000 Jan 22;9(2):217-26 [10607832.001]
  • [Cites] J Mol Histol. 2005 Jun;36(5):337-44 [16283426.001]
  • [Cites] Trends Cell Biol. 2005 Dec;15(12):651-8 [16243528.001]
  • [Cites] EMBO J. 2005 Dec 7;24(23):4018-28 [16281057.001]
  • [Cites] J Biol Chem. 2005 Dec 16;280(50):41207-12 [16230350.001]
  • [Cites] J Biol Chem. 2005 Dec 23;280(51):42252-62 [16203725.001]
  • [Cites] Exp Cell Res. 2006 Feb 15;312(4):478-87 [16337940.001]
  • [Cites] Nature. 2005 Dec 22;438(7071):1116-22 [16222246.001]
  • [Cites] J Cell Sci. 2006 Jan 15;119(Pt 2):239-49 [16410549.001]
  • [Cites] Genes Dev. 2006 Feb 15;20(4):486-500 [16481476.001]
  • [Cites] Mol Biol Cell. 2006 Mar;17(3):1154-63 [16371512.001]
  • [Cites] Brain. 2006 Apr;129(Pt 4):996-1013 [16478798.001]
  • [Cites] Curr Biol. 2006 Apr 18;16(8):825-31 [16631592.001]
  • [Cites] Semin Cancer Biol. 2006 Jun;16(3):203-13 [16725345.001]
  • [Cites] FEBS J. 2006 Jul;273(14):3204-15 [16857009.001]
  • [Cites] EMBO J. 2006 Jul 26;25(14):3275-85 [16858403.001]
  • [Cites] Curr Opin Cell Biol. 2002 Jun;14(3):357-64 [12067659.001]
  • [Cites] Nat Rev Mol Cell Biol. 2002 Aug;3(8):575-85 [12154369.001]
  • [Cites] FEBS Lett. 2002 Aug 14;525(1-3):135-40 [12163176.001]
  • [Cites] J Cell Biol. 2002 Aug 5;158(3):475-85 [12163470.001]
  • [Cites] J Biol Chem. 2002 Nov 8;277(45):43288-300 [12215455.001]
  • [Cites] Acta Haematol. 2002;108(4):210-8 [12432217.001]
  • [Cites] Dev Cell. 2002 Nov;3(5):659-71 [12431373.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Jan 17;300(3):679-85 [12507503.001]
  • [Cites] J Cell Sci. 2003 Mar 1;116(Pt 5):823-35 [12571280.001]
  • [Cites] J Biol Chem. 2003 Feb 28;278(9):6969-75 [12493765.001]
  • [Cites] EMBO J. 2003 Mar 17;22(6):1336-46 [12628926.001]
  • [Cites] Muscle Nerve. 2003 Apr;27(4):393-406 [12661041.001]
  • [Cites] J Biol Chem. 2003 Apr 18;278(16):14394-400 [12566455.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4598-603 [12684533.001]
  • [Cites] J Neurol Sci. 2003 Jun 15;210(1-2):47-51 [12736087.001]
  • [Cites] EMBO J. 2003 May 15;22(10):2324-33 [12743027.001]
  • [Cites] Eur J Biochem. 2003 Jun;270(11):2459-66 [12755701.001]
  • [Cites] Hum Mol Genet. 2003 Jun 1;12(11):1301-12 [12761045.001]
  • [Cites] Neuromuscul Disord. 2003 Aug;13(6):508-15 [12899879.001]
  • [Cites] Science. 2003 Sep 5;301(5638):1380-2 [12958361.001]
  • [Cites] Annu Rev Biochem. 2003;72:573-608 [14527325.001]
  • [Cites] EMBO J. 2003 Nov 3;22(21):5928-40 [14592989.001]
  • [Cites] Nat Cell Biol. 2004 Feb;6(2):97-105 [14743216.001]
  • [Cites] Anat Rec A Discov Mol Cell Evol Biol. 2006 Jul;288(7):676-80 [16761279.001]
  • [Cites] Biochem Cell Biol. 2006 Aug;84(4):418-26 [16936815.001]
  • [Cites] FEBS J. 2006 Oct;273(19):4562-75 [16972941.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Oct;7(10):782-8 [16926857.001]
  • [Cites] Hum Mol Genet. 2006 Dec 1;15(23):3459-72 [17067998.001]
  • [Cites] Trends Cell Biol. 2007 Apr;17(4):202-8 [17320395.001]
  • [Cites] J Biol Chem. 2007 May 11;282(19):14525-35 [17355960.001]
  • [Cites] Exp Cell Res. 2007 Aug 1;313(13):2845-57 [17462627.001]
  • [Cites] Eur J Biochem. 2004 Mar;271(5):1035-45 [15009215.001]
  • [Cites] Curr Opin Cell Biol. 2004 Feb;16(1):61-7 [15037306.001]
  • [Cites] Curr Opin Cell Biol. 2004 Feb;16(1):73-9 [15037308.001]
  • [Cites] Trends Cell Biol. 2004 May;14(5):261-6 [15130582.001]
  • [Cites] Mol Cell. 2004 Jun 4;14(5):685-91 [15175163.001]
  • [Cites] Genome Res. 2004 Jul;14(7):1315-23 [15231747.001]
  • [Cites] J Biol Chem. 2004 Jul 16;279(29):30856-64 [15123707.001]
  • [Cites] J Biol Chem. 2004 Aug 27;279(35):37175-84 [15220328.001]
  • [Cites] Curr Biol. 2004 Aug 24;14(16):1436-50 [15324660.001]
  • [Cites] PLoS Biol. 2004 Sep;2(9):E231 [15328537.001]
  • [Cites] Prog Clin Biol Res. 1990;327:141-8 [2138789.001]
  • [Cites] J Biol Chem. 1990 Jun 15;265(17):10148-55 [2161834.001]
  • [Cites] J Biochem. 1990 Nov;108(5):835-8 [2150518.001]
  • [Cites] Biochem J. 1991 Nov 15;280 ( Pt 1):33-8 [1835840.001]
  • [Cites] Genetics. 1993 Feb;133(2):361-73 [8382178.001]
  • [Cites] Biochem Biophys Res Commun. 1995 Dec 5;217(1):238-44 [8526917.001]
  • [Cites] Nat Genet. 1996 Mar;12(3):254-9 [8589715.001]
  • [Cites] J Biol Chem. 1996 Jun 21;271(25):14653-6 [8663349.001]
  • [Cites] Neuromuscul Disord. 2000 Jun;10(4-5):228-32 [10838246.001]
  • [Cites] J Biol Chem. 2000 Jun 23;275(25):18871-8 [10770926.001]
  • [Cites] Mol Cell. 2000 Apr;5(4):671-82 [10882103.001]
  • [Cites] Science. 2000 Oct 13;290(5490):337-41 [11030652.001]
  • [Cites] Nature. 2000 Nov 16;408(6810):377-81 [11099047.001]
  • [Cites] J Biol Chem. 2000 Dec 22;275(51):40463-70 [11013263.001]
  • [Cites] Trends Biochem Sci. 2001 Jan;26(1):41-7 [11165516.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1454-8 [11171972.001]
  • [Cites] J Cell Biol. 2001 Mar 5;152(5):895-910 [11238447.001]
  • [Cites] Curr Opin Cell Biol. 2001 Jun;13(3):274-80 [11343897.001]
  • [Cites] Biochemistry. 2001 Jun 19;40(24):7025-34 [11401546.001]
  • [Cites] FEBS Lett. 2001 Jul 20;501(2-3):171-6 [11470279.001]
  • [Cites] EMBO J. 2001 Aug 15;20(16):4399-407 [11500367.001]
  • [Cites] J Cell Biol. 2001 Sep 3;154(5):1019-30 [11535620.001]
  • [Cites] Am J Hum Genet. 2001 Nov;69(5):1033-45 [11590545.001]
  • [Cites] J Cell Sci. 2001 Sep;114(Pt 18):3297-307 [11591818.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):90-4 [11752412.001]
  • [Cites] J Cell Sci. 2001 Dec;114(Pt 24):4567-73 [11792821.001]
  • [Cites] J Cell Sci. 2001 Dec;114(Pt 24):4575-85 [11792822.001]
  • [Cites] Science. 2002 Mar 15;295(5562):2080-3 [11859155.001]
  • [Cites] Mol Cell. 2002 Mar;9(3):611-23 [11931768.001]
  • [Cites] Annu Rev Biochem. 2002;71:755-81 [12045110.001]
  • [Cites] J Cell Biol. 2002 Jun 10;157(6):929-39 [12045181.001]
  • [Cites] Cell. 1997 May 2;89(3):357-64 [9150135.001]
  • [Cites] J Biol Chem. 1997 Jul 4;272(27):17176-81 [9202039.001]
  • [Cites] J Biol Chem. 1997 Nov 7;272(45):28695-703 [9353338.001]
  • [Cites] Trends Biochem Sci. 1998 May;23(5):174-8 [9612081.001]
  • [Cites] Mol Cell. 1998 Dec;2(6):851-61 [9885572.001]
  • [Cites] Nature. 1999 Apr 29;398(6730):824-8 [10235266.001]
  • [Cites] J Cell Sci. 1999 Aug;112 ( Pt 15):2571-82 [10393813.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Aug 17;96(17):9873-8 [10449787.001]
  • [Cites] Nat Cell Biol. 2004 Dec;6(12):1165-72 [15558034.001]
  • [Cites] Mol Cell Biol. 2005 Jan;25(1):512-22 [15601870.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Jan;6(1):21-31 [15688064.001]
  • [Cites] Nat Genet. 2005 Mar;37(3):254-64 [15696166.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 1;102(9):3290-5 [15728376.001]
  • [Cites] Oncogene. 2005 Mar 3;24(10):1698-710 [15674337.001]
  • [Cites] J Biol Chem. 2005 Apr 8;280(14):13863-70 [15681850.001]
  • (PMID = 17620012.001).
  • [ISSN] 0006-2960
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / F32 GM067397-02; United States / NIGMS NIH HHS / GM / R01 GM048646-07; United States / NCRR NIH HHS / RR / 1S10-RR14702; United States / NIGMS NIH HHS / GM / GM048646-07; United States / NIGMS NIH HHS / GM / GM067397-02; United States / NIGMS NIH HHS / GM / F32GM067397; United States / NIGMS NIH HHS / GM / F32 GM067397; United States / NIGMS NIH HHS / GM / R01 GM048646; United States / NIGMS NIH HHS / GM / R01GM48646
  • [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 / Adaptor Proteins, Signal Transducing; 0 / Chromatin; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Multiprotein Complexes; 0 / Nuclear Matrix-Associated Proteins; 0 / Nuclear Proteins; 0 / Proteome; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors; 0 / emerin
  • [Other-IDs] NLM/ NIHMS62576; NLM/ PMC2635128
  •  go-up   go-down


66. Capek P, Brdicka R: Hypertrophic cardiomyopathy. Cas Lek Cesk; 2006;145(2):93-6; discussion 96-7
Genetic Alliance. consumer health - Hypertrophic Cardiomyopathy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hypertrophic cardiomyopathy is a multigenetic cardiac disease with autosomal dominant pattern of inheritance and incomplete penetrance, with the exclusion of those cases caused by mutations in the mitochondrial genome.
  • The disease is usually caused by mutations in several sarcomeric contractile protein genes.
  • Mutations have been found in four genes that encode components of the thick filament: beta myosin heavy chain (5), essential myosin light chains (6), regulatory myosin light chains (6), and cardiac myosin binding protein -C (7), (8); in five genes that encode thin filament proteins: cardiac actin (9), cardiac troponin T (10), cardiac troponin C (11), cardiac troponin I (12), and alpha-tropomyosin (10); and in the sarcomeric cytoskeletal protein titin (13).
  • In addition to mutations in contractile sarcomeric proteins, mutations in other genes encoding for non-sarcomeric proteins also have been identified in patients with-non pure form of hypertrophic cardiomyopathy.
  • As a complex cardiac disease, hypertrophic cardiomyopathy has unique pathophysiological characteristics and a various morphological, functional, and clinical features.

  • Genetic Alliance. consumer health - Cardiomyopathy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16521396.001).
  • [ISSN] 0008-7335
  • [Journal-full-title] Casopís lékar̆ů c̆eských
  • [ISO-abbreviation] Cas. Lek. Cesk.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Czech Republic
  • [Number-of-references] 35
  •  go-up   go-down


67. Edes IF, Tóth A, Csányi G, Lomnicka M, Chłopicki S, Edes I, Papp Z: Late-stage alterations in myofibrillar contractile function in a transgenic mouse model of dilated cardiomyopathy (Tgalphaq*44). J Mol Cell Cardiol; 2008 Sep;45(3):363-72
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.
  • These mechanical alterations were paralleled by a robust increase in beta-myosin heavy chain expression in the Tgalphaq*44 hearts.
  • [MeSH-major] Cardiomyopathy, Dilated / genetics. Disease Models, Animal. GTP-Binding Protein alpha Subunits, Gq-G11 / genetics. Models, Cardiovascular. Myocardial Contraction / physiology. Myofibrils / 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
  • (PMID = 18674539.001).
  • [ISSN] 1095-8584
  • [Journal-full-title] Journal of molecular and cellular cardiology
  • [ISO-abbreviation] J. Mol. Cell. Cardiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gq-G11
  •  go-up   go-down


68. Puri P, Mirshahi F, Cheung O, Natarajan R, Maher JW, Kellum JM, Sanyal AJ: Activation and dysregulation of the unfolded protein response in nonalcoholic fatty liver disease. Gastroenterology; 2008 Feb;134(2):568-76
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] Activation and dysregulation of the unfolded protein response in nonalcoholic fatty liver disease.
  • Liver histology was scored using the NASH clinical research network criteria.
  • Whereas immunoglobulin heavy chain binding protein mRNA was significantly increased in NASH, unspliced X-box protein-1 (XBP-1) protein did not increase.
  • Also, endoplasmic reticulum degradation-enhancing alpha-mannosidase-like protein mRNA levels were inversely related to spliced XBP-1 mRNA in NASH.

  • Genetic Alliance. consumer health - Liver Disease.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • 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 = 18082745.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K24 DK 02755-07; United States / PHS HHS / / R01 56331; United States / NIDDK NIH HHS / DK / T32 DK 007150-32
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATF4 protein, human; 0 / ATF6 protein, human; 0 / Activating Transcription Factor 6; 0 / Antigens, Differentiation; 0 / Cell Cycle Proteins; 0 / DDIT3 protein, human; 0 / DNA-Binding Proteins; 0 / Eukaryotic Initiation Factor-2; 0 / Membrane Proteins; 0 / Transcription Factors; 0 / regulatory factor X transcription factors; 145891-90-3 / Activating Transcription Factor 4; 147336-12-7 / Transcription Factor CHOP; EC 2.7.1.- / ERN2 protein, human; EC 2.7.10.- / PERK kinase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / eIF-2 Kinase; EC 2.7.12.2 / MAP Kinase Kinase 4; EC 3.1.- / Endoribonucleases; EC 3.1.3.16 / PPP1R15A protein, human; EC 3.1.3.16 / Protein Phosphatase 1
  •  go-up   go-down


69. Degens H, Swisher AK, Heijdra YF, Siu PM, Dekhuijzen PN, Alway SE: Apoptosis and Id2 expression in diaphragm and soleus muscle from the emphysematous hamster. Am J Physiol Regul Integr Comp Physiol; 2007 Jul;293(1):R135-44
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • During chronic obstructive pulmonary disease (COPD) diaphragm and peripheral muscle weakness occur.
  • The mRNA levels of TNF-alpha and markers of apoptosis were significantly elevated in the diaphragm and soleus muscles during emphysema.
  • Thus, despite the absence of muscle atrophy in emphysematous hamsters, there was evidence of increased TNF-alpha expression, apoptosis, and altered muscle-specific transcriptional regulation as reflected by decreased MyoD and elevated Id2 levels at least in the soleus and diaphragm muscle.
  • [MeSH-minor] Animals. Caspase 3 / metabolism. Cell Nucleus / metabolism. Cricetinae. Cytosol / metabolism. DNA Fragmentation. Male. Mesocricetus. Muscle Fibers, Skeletal / chemistry. Muscle Fibers, Skeletal / physiology. MyoD Protein / genetics. Myosin Heavy Chains / metabolism. NF-kappa B / biosynthesis. Pulmonary Disease, Chronic Obstructive / metabolism. Pulmonary Disease, Chronic Obstructive / pathology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / biosynthesis

  • MedlinePlus Health Information. consumer health - Emphysema.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17395785.001).
  • [ISSN] 0363-6119
  • [Journal-full-title] American journal of physiology. Regulatory, integrative and comparative physiology
  • [ISO-abbreviation] Am. J. Physiol. Regul. Integr. Comp. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Inhibitor of Differentiation Protein 2; 0 / MyoD Protein; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.- / Caspase 3; EC 3.6.4.1 / Myosin Heavy Chains
  •  go-up   go-down


70. Heitner JC, Koy C, Kreutzer M, Gerber B, Reimer T, Glocker MO: Differentiation of HELLP patients from healthy pregnant women by proteome analysis--on the way towards a clinical marker set. J Chromatogr B Analyt Technol Biomed Life Sci; 2006 Aug 7;840(1):10-9
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] Differentiation of HELLP patients from healthy pregnant women by proteome analysis--on the way towards a clinical marker set.
  • A specific plasma protein profile for the HELLP-syndrome was generated involving protein areas that contain inter-alpha-trypsin inhibitor heavy chain H4, kininogen 1, fibrinogen gamma chain, transthyretin, haptoglobins, and serum amyloid A with statistically significant expression differences when compared to controls.
  • It now is possible to clinically elucidate if the differentially expressed proteins are suited for longitudinal studies concerning both, to function as markers or perhaps even as disease predictors that might become relevant for diagnostic tests.

  • 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 = 16837253.001).
  • [ISSN] 1570-0232
  • [Journal-full-title] Journal of chromatography. B, Analytical technologies in the biomedical and life sciences
  • [ISO-abbreviation] J. Chromatogr. B Analyt. Technol. Biomed. Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Proteome
  •  go-up   go-down


71. Kirstein F, Horsnell WG, Kuperman DA, Huang X, Erle DJ, Lopata AL, Brombacher F: Expression of IL-4 receptor alpha on smooth muscle cells is not necessary for development of experimental allergic asthma. J Allergy Clin Immunol; 2010 Aug;126(2):347-54
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of IL-4 receptor alpha on smooth muscle cells is not necessary for development of experimental allergic asthma.
  • In vitro studies have suggested that IL-4 receptor alpha (IL-4Ralpha) signaling on smooth muscle cells is critical for airway inflammation and airway hyperresponsiveness.
  • METHODS: By using transgenic smooth muscle myosin heavy chain(cre)IL-4Ralpha(-/lox) mice deficient in IL-4Ralpha in smooth muscle cells, in vivo effects of impaired IL-4Ralpha signaling in smooth muscle cells on the outcome of asthmatic disease were investigated for the first time.
  • Mice were investigated for the presence of airway hyperresponsiveness, airway inflammation, allergen-specific antibody production, T(h)2-type cytokine responses, and lung pathology.
  • RESULTS: Airway hyperresponsiveness, airway inflammation, mucus production, T(h)2 cytokine production, and specific antibody responses were unaffected in smooth muscle myosin heavy chain(cre)IL-4Ralpha(-/lox) mice compared with control animals.
  • These findings suggest that IL-4Ralpha responsiveness in airway smooth muscle cells during the early phase of allergic asthma is not, as suggested, necessary for the outcome of the disease.

  • MedlinePlus Health Information. consumer health - Asthma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
  • [Cites] J Immunol. 1999 Mar 1;162(5):2477-87 [10072486.001]
  • [Cites] Science. 1998 Dec 18;282(5397):2261-3 [9856950.001]
  • [Cites] J Immunol. 1999 May 15;162(10):6178-83 [10229862.001]
  • [Cites] J Immunol. 1999 Jun 15;162(12):7302-8 [10358179.001]
  • [Cites] J Allergy Clin Immunol. 2005 Mar;115(3):514-20 [15753898.001]
  • [Cites] J Immunol. 2005 Sep 15;175(6):3746-52 [16148120.001]
  • [Cites] PLoS Pathog. 2007 Jan;3(1):e1 [17222057.001]
  • [Cites] J Allergy Clin Immunol. 2008 Feb;121(2):334-5 [18177698.001]
  • [Cites] Circ Res. 2000 Sep 1;87(5):363-9 [10969033.001]
  • [Cites] Am J Respir Cell Mol Biol. 2001 Jun;24(6):755-61 [11415942.001]
  • [Cites] Am J Respir Crit Care Med. 2001 Jul 1;164(1):141-8 [11435252.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2002 Feb;282(2):G226-32 [11804843.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2002 Mar;282(3):L520-8 [11839548.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2002 Apr;282(4):L847-53 [11880312.001]
  • [Cites] Am J Respir Crit Care Med. 2002 Apr 15;165(8):1161-71 [11956062.001]
  • [Cites] Nat Med. 2002 Aug;8(8):885-9 [12091879.001]
  • [Cites] J Allergy Clin Immunol. 2003 Jun;111(6):1307-18 [12789234.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2003 Oct;285(4):L907-14 [12871855.001]
  • [Cites] Br J Pharmacol. 2003 Dec;140(7):1159-62 [14597600.001]
  • [Cites] Am J Respir Crit Care Med. 2004 Mar 1;169(5):596-603 [14670803.001]
  • [Cites] Immunity. 2004 May;20(5):623-35 [15142530.001]
  • [Cites] Clin Exp Allergy. 2004 Aug;34(8):1291-8 [15298572.001]
  • [Cites] J Allergy Clin Immunol. 2004 Aug;114(2 Suppl):S32-50 [15309017.001]
  • [Cites] J Allergy Clin Immunol. 2004 Oct;114(4):791-8 [15480317.001]
  • [Cites] J Immunol Methods. 1985 Nov 7;83(2):209-15 [3840509.001]
  • [Cites] Am J Respir Cell Mol Biol. 1995 Jul;13(1):54-9 [7598937.001]
  • [Cites] J Exp Med. 1996 Jan 1;183(1):109-17 [8551213.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jul 23;93(15):7821-5 [8755560.001]
  • [Cites] J Exp Med. 1997 Jun 16;185(12):2143-56 [9182686.001]
  • [Cites] Am J Respir Crit Care Med. 1997 Sep;156(3 Pt 1):766-75 [9309991.001]
  • [Cites] J Immunol. 1998 Apr 15;160(8):4004-9 [9558109.001]
  • [Cites] J Exp Med. 1998 Oct 5;188(7):1307-20 [9763610.001]
  • [Cites] Science. 1998 Dec 18;282(5397):2258-61 [9856949.001]
  • [Cites] J Clin Invest. 1999 Mar;103(6):779-88 [10079098.001]
  • (PMID = 20579713.001).
  • [ISSN] 1097-6825
  • [Journal-full-title] The Journal of allergy and clinical immunology
  • [ISO-abbreviation] J. Allergy Clin. Immunol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL085089-05; United States / NHLBI NIH HHS / HL / R01 HL085089; United States / NHLBI NIH HHS / HL / HL56835; United States / NHLBI NIH HHS / HL / R01 HL085089-05; United Kingdom / Wellcome Trust / /
  • [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 / Allergens; 0 / Biomarkers; 0 / Il4ra protein, mouse; 0 / Interleukin-13; 0 / Receptors, Cell Surface; 207137-56-2 / Interleukin-4
  • [Other-IDs] NLM/ NIHMS204346; NLM/ PMC2917502
  •  go-up   go-down


72. Girolami F, Ho CY, Semsarian C, Baldi M, Will ML, Baldini K, Torricelli F, Yeates L, Cecchi F, Ackerman MJ, Olivotto I: Clinical features and outcome of hypertrophic cardiomyopathy associated with triple sarcomere protein gene mutations. J Am Coll Cardiol; 2010 Apr 6;55(14):1444-53
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] Clinical features and outcome of hypertrophic cardiomyopathy associated with triple sarcomere protein gene mutations.
  • OBJECTIVES: The aim of this study was to describe the clinical profile associated with triple sarcomere gene mutations in a large hypertrophic cardiomyopathy (HCM) cohort.
  • BACKGROUND: In patients with HCM, double or compound sarcomere gene mutation heterozygosity might be associated with earlier disease onset and more severe outcome.
  • METHODS: A total of 488 unrelated index HCM patients underwent screening for myofilament gene mutations by direct deoxyribonucleic acid sequencing of 8 genes, including myosin binding protein C (MYBPC3), beta-myosin heavy chain (MYH7), regulatory and essential light chains (MYL2, MYL3), troponin-T (TNNT2), troponin-I (TNNI3), alpha-tropomyosin (TPM1), and actin (ACTC).
  • The fourth patient, however, had clinically mild disease.

  • Genetic Alliance. consumer health - Cardiomyopathy.
  • Genetic Alliance. consumer health - Hypertrophic Cardiomyopathy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
  • [CommentIn] J Am Coll Cardiol. 2010 Apr 6;55(14):1454-5 [20359595.001]
  • (PMID = 20359594.001).
  • [ISSN] 1558-3597
  • [Journal-full-title] Journal of the American College of Cardiology
  • [ISO-abbreviation] J. Am. Coll. Cardiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


73. Zhou C, Fu X, Yan J, Fan Q, Li Z, Cianflone K, Wang D: Throat infection, neck and chest pain and cardiac response: a persistent infection-related clinical syndrome. J Huazhong Univ Sci Technolog Med Sci; 2009 Feb;29(1):19-24
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] Throat infection, neck and chest pain and cardiac response: a persistent infection-related clinical syndrome.
  • Dizziness, chest discomfort, chest depression and dyspnea are a group of symptoms that are common complaints in clinical practice.
  • Patients with these symptoms are usually informed that while neurosis consequent to coronary heart disease is excluded nonetheless they remain unhealthy with no rational explanation or treatment.
  • Thirty-five patients received coronary artery angiography to exclude coronary heart disease.
  • Serum myocardial autoantibodies against beta(1)-adrenoceptor, alpha-myosin heavy chain, M(2)-muscarinic receptor and adenine-nucleotide translocator were tested, and inflammatory cytokines and high sensitivity C-reaction protein were measured and lymphocyte subclass was assayed by flow cytometry.
  • TNF-alpha, IL-1 and IL-6 were significantly higher in patients than in controls (P<0.01).
  • These data led to identification of a persistent respiratory infection-related clinical syndrome, including persistent throat infection, neck spinal lesion, rib cartilage inflammation, symptoms of cardiac depression and dyspnea with or without anxiety.
  • [MeSH-major] Chest Pain / diagnosis. Coronary Disease / diagnosis. Dyspnea / diagnosis. Neck Pain / diagnosis. Pharyngitis / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Diagnosis, Differential. Dizziness / complications. Dizziness / diagnosis. Female. Humans. Male. Middle Aged. Prospective Studies. Syndrome. Virus Diseases / complications. Virus Diseases / diagnosis. Young Adult

  • MedlinePlus Health Information. consumer health - Breathing Problems.
  • MedlinePlus Health Information. consumer health - Chest Pain.
  • MedlinePlus Health Information. consumer health - Neck Injuries and Disorders.
  • MedlinePlus Health Information. consumer health - Sore Throat.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19224156.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


74. Machado MV, Martins A, Almeida R, Marques-Vidal P, Gonçalves MS, Camilo ME, Cortez-Pinto H: Does the simultaneous tumor necrosis factor receptor 2, tumor necrosis factor promoter gene polymorphism represent a higher risk for alcoholic liver disease? Eur J Gastroenterol Hepatol; 2009 Feb;21(2):201-5
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] Does the simultaneous tumor necrosis factor receptor 2, tumor necrosis factor promoter gene polymorphism represent a higher risk for alcoholic liver disease?
  • BACKGROUND AND AIM: Tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine that seems to play a crucial role in the pathogenesis of alcoholic liver disease (ALD).
  • TNF-alpha exerts its effects by binding to specific receptors (TNFR); the polymorphism of TNFRII T587G has been associated with increased TNF apoptotic response and its presence may increase the risk to develop liver disease.
  • The aim of this study was to evaluate the prevalence of the TNF-alpha G238A promoter and TNFRII polymorphisms, individually or simultaneously, in ALD.
  • METHODS: TNF-alpha G238A and TNFRII T587G polymorphisms were studied in 103 unrelated patients with ALD (biopsy confirmed or clinical evidence) and in 76 heavy drinkers without liver disease (NLD).
  • Single nucleotide polymorphism gene was detected by a polymerase chain reaction-restriction fragment length polymorphisms method.
  • RESULTS: TNF-alpha G238A allele frequency was similar in both groups.
  • TNF-alpha G238A and TNFRII T587G were simultaneously present in six ALD patients and in none of NLD patients (P=0.04).
  • CONCLUSION: Although individually there was no association between TNFRII T587G or TNF-alpha G238A polymorphisms and ALD, this study suggests that the presence of both polymorphisms may enhance the susceptibility for ALD.
  • TNF-alpha G238A may increase TNF-alpha production, which when associated with TNFRII T587G, can further exacerbate TNF-alpha response leading to a greater risk of ALD.
  • [MeSH-major] Liver Diseases, Alcoholic / genetics. Polymorphism, Genetic. Receptors, Tumor Necrosis Factor, Type II / genetics. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adult. Female. Gene Frequency. Genetic Predisposition to Disease. Humans. Male. Middle Aged. Promoter Regions, Genetic / genetics

  • Genetic Alliance. consumer health - Liver Disease.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19212208.001).
  • [ISSN] 1473-5687
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


75. Lombardi R, Rodriguez G, Chen SN, Ripplinger CM, Li W, Chen J, Willerson JT, Betocchi S, Wickline SA, Efimov IR, Marian AJ: Resolution of established cardiac hypertrophy and fibrosis and prevention of systolic dysfunction in a transgenic rabbit model of human cardiomyopathy through thiol-sensitive mechanisms. Circulation; 2009 Mar 17;119(10):1398-407
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.
  • BACKGROUND: Cardiac hypertrophy, the clinical hallmark of hypertrophic cardiomyopathy (HCM), is a major determinant of morbidity and mortality not only in HCM but also in a number of cardiovascular diseases.
  • METHODS AND RESULTS: We treated 2-year-old beta-myosin heavy-chain Q403 transgenic rabbits with established cardiac hypertrophy and preserved systolic function with N-acetylcysteine or a placebo for 12 months (n=10 per group).
  • Transgenic rabbits in the placebo group had cardiac hypertrophy, fibrosis, systolic dysfunction, increased oxidized to total glutathione ratio, higher levels of activated thiol-sensitive active protein kinase G, dephosphorylated nuclear factor of activated T cells (NFATc1) and phospho-p38, and reduced levels of glutathiolated cardiac alpha-actin.
  • Treatment with N-acetylcysteine restored oxidized to total glutathione ratio, normalized levels of glutathiolated cardiac alpha-actin, reversed cardiac and myocyte hypertrophy and interstitial fibrosis, reduced the propensity for ventricular arrhythmias, prevented cardiac dysfunction, restored myocardial levels of active protein kinase G, and dephosphorylated NFATc1 and phospho-p38.
  • Because there is no effective pharmacological therapy for HCM and given that hypertrophy, fibrosis, and cardiac dysfunction are common and major predictors of clinical outcomes, the findings could have implications in various cardiovascular disorders.

  • Genetic Alliance. consumer health - Cardiomyopathy.
  • MedlinePlus Health Information. consumer health - Antioxidants.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. N-ACETYLCYSTEINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Mol Cell Cardiol. 2004 May;36(5):663-73 [15135661.001]
  • [Cites] Curr Opin Cardiol. 2008 May;23(3):199-205 [18382207.001]
  • [Cites] J Clin Invest. 1999 Dec;104(12):1683-92 [10606622.001]
  • [Cites] N Engl J Med. 2000 Jun 15;342(24):1778-85 [10853000.001]
  • [Cites] Circulation. 2000 Sep 19;102(12):1346-50 [10993850.001]
  • [Cites] Eur J Clin Invest. 2000 Oct;30(10):915-29 [11029607.001]
  • [Cites] J Appl Physiol (1985). 2001 Apr;90(4):1299-306 [11247927.001]
  • [Cites] Circulation. 2001 Jul 17;104(3):317-24 [11457751.001]
  • [Cites] JAMA. 2002 Mar 13;287(10):1308-20 [11886323.001]
  • [Cites] Circulation. 2002 Mar 26;105(12):1503-8 [11914262.001]
  • [Cites] J Biol Chem. 2003 Jan 3;278(1):679-85 [12409293.001]
  • [Cites] Cell Mol Life Sci. 2003 Jan;60(1):6-20 [12613655.001]
  • [Cites] Cell. 2003 May 2;113(3):329-42 [12732141.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2003 Sep;285(3):H946-54 [12763752.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2004 Jan;286(1):L121-8 [12959930.001]
  • [Cites] J Biol Chem. 1980 Jun 25;255(12):5668-73 [6247341.001]
  • [Cites] N Engl J Med. 1990 May 31;322(22):1561-6 [2139921.001]
  • [Cites] J Am Coll Cardiol. 1998 Nov;32(5):1454-9 [9809962.001]
  • [Cites] Life Sci. 2005 May 27;77(2):175-82 [15862602.001]
  • [Cites] Free Radic Biol Med. 2005 Jun 1;38(11):1501-10 [15890624.001]
  • [Cites] Circ Res. 2005 Aug 5;97(3):285-92 [16020756.001]
  • [Cites] N Engl J Med. 2005 Nov 24;353(21):2229-42 [16306520.001]
  • [Cites] J Am Coll Cardiol. 2006 Feb 21;47(4):827-34 [16487852.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 21;103(12):4628-33 [16537378.001]
  • [Cites] J Cell Mol Med. 2006 Jan-Mar;10(1):157-65 [16563228.001]
  • [Cites] J Biol Chem. 2006 Aug 11;281(32):22983-91 [16757472.001]
  • [Cites] Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1819-27 [16987034.001]
  • [Cites] Hypertension. 2007 Feb;49(2):241-8 [17190878.001]
  • [Cites] Nat Protoc. 2006;1(4):1872-8 [17487171.001]
  • [Cites] Science. 2007 Jun 22;316(5832):1749-52 [17588931.001]
  • [Cites] Curr Opin Pharmacol. 2007 Aug;7(4):355-9 [17602868.001]
  • [Cites] J Clin Invest. 2007 Sep;117(9):2592-601 [17786245.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2007 Sep;293(3):H1969-77 [17573457.001]
  • [Cites] Science. 2007 Sep 7;317(5843):1393-7 [17717153.001]
  • [Cites] Circ Res. 2007 Nov 9;101(10):1049-57 [17885214.001]
  • [Cites] Crit Care Med. 2008 Feb;36(2):565-71 [18216605.001]
  • [Cites] N Engl J Med. 2008 Mar 27;358(13):1370-80 [18367740.001]
  • [Cites] Cardiovasc Res. 2004 Aug 15;63(3):467-75 [15276472.001]
  • (PMID = 19255346.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] ENG
  • [Grant] None / None / / R01 HL068884-04; None / None / / P50 HL054313-090012; United States / NHLBI NIH HHS / HL / P50 HL054313; United States / NHLBI NIH HHS / HL / R01 HL068884-02; None / None / / P50 HL054313-060012; United States / NHLBI NIH HHS / HL / R01 HL068884-04; United States / NIAMS NIH HHS / AR / R01 AR056223; United States / NHLBI NIH HHS / HL / R01 HL068884-01; United States / NHLBI NIH HHS / HL / P50 HL054313-080012; None / None / / R01 HL068884-03; United States / NHLBI NIH HHS / HL / R01-HL68884; United States / NHLBI NIH HHS / HL / R01 HL068884-03; United States / NHLBI NIH HHS / HL / R01 HL068884; United States / NHLBI NIH HHS / HL / P50 HL054313-070012; None / None / / P50 HL054313-100012; None / None / / P50 HL054313-08S10012; None / None / / P50 HL054313-080012; United States / NHLBI NIH HHS / HL / P50 HL054313-08S10012; United States / NHLBI NIH HHS / HL / R01 HL068884-05; United States / NHLBI NIH HHS / HL / P50 HL054313-090012; None / None / / R01 HL068884-05; None / None / / P50 HL054313-070012; None / None / / R01 HL068884-02; United States / NHLBI NIH HHS / HL / R01-HL67322; United States / NHLBI NIH HHS / HL / P50 HL054313-100012; United States / NHLBI NIH HHS / HL / R01 HL067322; United States / NHLBI NIH HHS / HL / P50 HL054313-060012; None / None / / R01 HL068884-01
  • [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 / Actins; 0 / Antioxidants; 0 / NFATC Transcription Factors; 0 / Sulfhydryl Compounds; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.6.4.1 / Myosin Heavy Chains; GAN16C9B8O / Glutathione; WYQ7N0BPYC / Acetylcysteine
  • [Other-IDs] NLM/ NIHMS113912; NLM/ PMC2773801
  •  go-up   go-down


76. Klaassen S, Probst S, Oechslin E, Gerull B, Krings G, Schuler P, Greutmann M, Hürlimann D, Yegitbasi M, Pons L, Gramlich M, Drenckhahn JD, Heuser A, Berger F, Jenni R, Thierfelder L: Mutations in sarcomere protein genes in left ventricular noncompaction. Circulation; 2008 Jun 3;117(22):2893-901
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Heterozygous mutations were identified in 11 of 63 samples in genes encoding beta-myosin heavy chain (MYH7), alpha-cardiac actin (ACTC), and cardiac troponin T (TNNT2).
  • Clinical evaluations demonstrated familial disease in 6 of 11 probands with sarcomere gene mutations.
  • MYH7 mutations segregated with the disease in 4 autosomal dominant LVNC kindreds.
  • Six of the MYH7 mutations were novel, and 1 encodes a splice-site mutation, a relatively unique finding for MYH7 mutations.
  • Modified residues in beta-myosin heavy chain were located mainly within the ATP binding site.
  • [MeSH-major] Actins / genetics. Cardiac Myosins / genetics. Cardiomyopathies / genetics. Heart Ventricles / abnormalities. Mutation. Myosin Heavy Chains / genetics. Sarcomeres / genetics. Troponin T / genetics

  • Genetics Home Reference. consumer health - TNNT2 gene.
  • MedlinePlus Health Information. consumer health - Cardiomyopathy.
  • SciCrunch. OMIM: Data: Gene Annotation .
  • SciCrunch. Clinical Genomic Database: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Circulation. 2008 Jun 3;117(22):2847-9 [18519860.001]
  • (PMID = 18506004.001).
  • [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 / ACTC1 protein, human; 0 / Actins; 0 / MYH7 protein, human; 0 / Troponin T; EC 3.6.1.- / Cardiac Myosins; EC 3.6.4.1 / Myosin Heavy Chains
  •  go-up   go-down


77. Koninckx R, Hensen K, Daniëls A, Moreels M, Lambrichts I, Jongen H, Clijsters C, Mees U, Steels P, Hendrikx M, Rummens JL: Human bone marrow stem cells co-cultured with neonatal rat cardiomyocytes display limited cardiomyogenic plasticity. Cytotherapy; 2009;11(6):778-92
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Stem cells were obtained from patients with ischemic heart disease.
  • Co-cultured stem cells were separated from NRCM by flow sorting, and cardiac gene expression was analyzed by reverse transcriptase-polymerase chain reaction.
  • However, no expression of alpha-actinin, myosin heavy chain or troponin I was detected.
  • However, no morphologic changes could be detected by immunofluorescence or by TEM.
  • These data could explain why only limited functional improvement was reported in clinical stem cell trials.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • Hazardous Substances Data Bank. DIMETHYL SULFOXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19878064.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cryoprotective Agents; 0 / Enzyme Inhibitors; 0 / GATA4 Transcription Factor; 0 / Troponin T; M801H13NRU / Azacitidine; YOW8V9698H / Dimethyl Sulfoxide
  •  go-up   go-down


78. Li XM, Ma YT, Yang YN, Liu F, Chen BD, Han W, Zhang JF, Gao XM: Downregulation of survival signalling pathways and increased apoptosis in the transition of pressure overload-induced cardiac hypertrophy to heart failure. Clin Exp Pharmacol Physiol; 2009 Nov;36(11):1054-61
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.
  • 4. Following TAC, mRNA levels of atrial natriuretic peptide, B-type natriuretic peptide, beta-myosin heavy chain (MHC) and transforming growth factor-beta1 were increased time dependently, whereas mRNA expression of alpha-MHC, sarcoplasmic/endoplasmic reticulum calcium ATPase 2a and Bcl-2 were decreased.
  • [MeSH-minor] Animals. Aorta / pathology. Apoptosis / physiology. Disease Models, Animal. Fibrosis / pathology. Gene Expression. Hemodynamics. Male. Mice. Mice, Inbred C57BL. Myocytes, Cardiac / metabolism. Myocytes, Cardiac / pathology. Organ Size. Phosphorylation

  • MedlinePlus Health Information. consumer health - Heart Failure.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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
  • [CommentIn] Clin Exp Pharmacol Physiol. 2010 Jan;37(1):10-1 [19650791.001]
  • (PMID = 19566828.001).
  • [ISSN] 1440-1681
  • [Journal-full-title] Clinical and experimental pharmacology & physiology
  • [ISO-abbreviation] Clin. Exp. Pharmacol. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins
  •  go-up   go-down


79. Tsoutsman T, Kelly M, Ng DC, Tan JE, Tu E, Lam L, Bogoyevitch MA, Seidman CE, Seidman JG, Semsarian C: Severe heart failure and early mortality in a double-mutation mouse model of familial hypertrophic cardiomyopathy. Circulation; 2008 Apr 8;117(14):1820-31
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Familial hypertrophic cardiomyopathy (FHC) is characterized by genetic and clinical heterogeneity.
  • Five percent of FHC families have 2 FHC-causing mutations, which results in earlier disease onset, increased cardiac dysfunction, and a higher incidence of sudden death events.
  • This model (designated TnI-203/MHC-403) was generated by crossbreeding mice with the Gly203Ser cardiac troponin I (TnI-203) and Arg403Gln alpha-myosin heavy chain (MHC-403) FHC-causing mutations.
  • Increased levels of phosphorylated STAT3 were observed in TnI-203/MHC-403 mice and corresponded with the onset of disease, which suggests a possible cardioprotective response.
  • The presence of 2 disease-causing mutations may predispose individuals to a greater risk of developing severe heart failure than human FHC caused by a single gene mutation.
  • [MeSH-major] Cardiomyopathy, Dilated / genetics. Cardiomyopathy, Hypertrophic, Familial / genetics. Disease Models, Animal. Mutation. Troponin I / genetics. Ventricular Myosins / genetics
  • [MeSH-minor] Animals. Calcium Signaling. Disease Progression. Female. Heterozygote. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Mutant Strains. Mutation, Missense. Paracrine Communication. Phenotype. Renin-Angiotensin System / physiology. STAT3 Transcription Factor / physiology. Signal Transduction


80. Krishnamoorthy G, Lassmann H, Wekerle H, Holz A: Spontaneous opticospinal encephalomyelitis in a double-transgenic mouse model of autoimmune T cell/B cell cooperation. J Clin Invest; 2006 Sep;116(9):2385-92
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.
  • We describe a double-transgenic mouse strain (opticospinal EAE [OSE] mouse) that spontaneously develops an EAE-like neurological syndrome closely resembling a human variant of multiple sclerosis, Devic disease (also called neuromyelitis optica).
  • Like in Devic disease, the inflammatory, demyelinating lesions were located in the optic nerve and spinal cord, sparing brain and cerebellum, and the murine lesions showed histological similarity with their human correlates.
  • OSE mice have recombination-competent immune cells expressing a TCR-alphabeta specific for myelin oligodendrocyte glycoprotein (MOG) aa 35-55 peptide in the context of I-Ab along with an Ig J region replaced by the recombined heavy chain of a monoclonal antibody binding to a conformational epitope on MOG.
  • [MeSH-minor] Animals. Autoimmunity. Cell Division. Crosses, Genetic. Disease Models, Animal. Immunoglobulin Heavy Chains / genetics. Lymphocyte Subsets / immunology. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Transgenic. Myelin Proteins. Myelin-Oligodendrocyte Glycoprotein. Optic Nerve / pathology. Receptors, Antigen, T-Cell, alpha-beta / genetics. Spinal Cord / pathology

  • COS Scholar Universe. author profiles.
  • 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).
  • 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] Lab Invest. 1997 Mar;76(3):355-64 [9121118.001]
  • [Cites] J Neuroimmunol. 1995 Dec;63(1):17-27 [8557821.001]
  • [Cites] J Exp Med. 1996 Dec 1;184(6):2271-8 [8976182.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1996 Apr;60(4):382-7 [8774400.001]
  • [Cites] Immunol Today. 1998 Mar;19(3):117-20 [9540270.001]
  • [Cites] Immunol Cell Biol. 1998 Feb;76(1):34-40 [9553774.001]
  • [Cites] J Exp Med. 1998 Jul 6;188(1):169-80 [9653093.001]
  • [Cites] J Immunol. 1998 Nov 1;161(9):4480-3 [9794370.001]
  • [Cites] Brain Pathol. 1998 Oct;8(4):681-94 [9804377.001]
  • [Cites] J Immunol. 1999 Nov 1;163(9):5133-44 [10528220.001]
  • [Cites] Lancet. 2004 Dec 11-17;364(9451):2106-12 [15589308.001]
  • [Cites] Neurology. 2005 Apr 12;64(7):1270-2 [15824362.001]
  • [Cites] Lancet. 2005 Aug 13-19;366(9485):579-82 [16099294.001]
  • [Cites] J Exp Med. 2005 Aug 15;202(4):473-7 [16087714.001]
  • [Cites] Eur J Immunol. 1999 Nov;29(11):3432-9 [10556797.001]
  • [Cites] J Immunol. 2000 Nov 1;165(9):5360-6 [11046072.001]
  • [Cites] Trends Mol Med. 2001 Mar;7(3):115-21 [11286782.001]
  • [Cites] J Exp Med. 2001 Jun 18;193(12):F47-50 [11413199.001]
  • [Cites] J Clin Invest. 2001 Dec;108(12):1749-58 [11748258.001]
  • [Cites] N Engl J Med. 2002 Sep 19;347(12):911-20 [12239261.001]
  • [Cites] Nat Rev Immunol. 2003 Mar;3(3):189-98 [12658267.001]
  • [Cites] Curr Opin Rheumatol. 2003 May;15(3):246-52 [12707577.001]
  • [Cites] J Exp Med. 2003 May 5;197(9):1073-81 [12732654.001]
  • [Cites] Lab Invest. 2003 Jul;83(7):1081-8 [12861047.001]
  • [Cites] J Clin Invest. 2003 Aug;112(4):544-53 [12925695.001]
  • [Cites] J Immunol. 2003 Sep 1;171(5):2725-33 [12928426.001]
  • [Cites] J Clin Invest. 2004 Apr;113(7):990-7 [15057305.001]
  • [Cites] J Immunol. 2004 Apr 15;172(8):4686-90 [15067043.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 26;101(43):15434-9 [15492218.001]
  • [Cites] Curr Opin Immunol. 2004 Dec;16(6):808-14 [15511677.001]
  • [Cites] Neuropathol Appl Neurobiol. 1980 Jan-Feb;6(1):9-21 [6769061.001]
  • [Cites] Cell Immunol. 1982 Sep 15;72(2):360-6 [6185236.001]
  • [Cites] J Neuroimmunol. 1984 Sep-Oct;6(6):387-96 [6207204.001]
  • [Cites] Cell. 1987 Sep 11;50(6):819-20 [3621346.001]
  • [Cites] Am J Pathol. 1988 Mar;130(3):443-54 [2450462.001]
  • [Cites] Annu Rev Immunol. 1990;8:773-93 [2188679.001]
  • [Cites] J Neuroimmunol. 1992 Nov;41(1):1-8 [1281165.001]
  • [Cites] Cell. 1993 Feb 26;72(4):551-60 [7679952.001]
  • [Cites] Immunol Today. 1993 May;14(5):193-6 [8517916.001]
  • [Cites] Clin Microbiol Rev. 1993 Oct;6(4):382-427 [8269393.001]
  • [Cites] Cell. 1994 Aug 12;78(3):399-408 [7520367.001]
  • [CommentIn] J Clin Invest. 2006 Sep;116(9):2313-6 [16955130.001]
  • (PMID = 16955140.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / MOG protein, human; 0 / Mog protein, mouse; 0 / Myelin Proteins; 0 / Myelin-Associated Glycoprotein; 0 / Myelin-Oligodendrocyte Glycoprotein; 0 / Receptors, Antigen, T-Cell, alpha-beta
  • [Other-IDs] NLM/ PMC1555668
  •  go-up   go-down


81. Nagi B, Rana SS, Kochhar R, Bhasin DK: Sonoenteroclysis: a new technique for the diagnosis of small bowel diseases. Abdom Imaging; 2006 Jul-Aug;31(4):417-24
Hazardous Substances Data Bank. Barium sulfate .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sonoenteroclysis: a new technique for the diagnosis of small bowel diseases.
  • BACKGROUND: Radiologic evaluation of small bowel is usually done by barium examination, which involves considerable radiation exposure.
  • A new sonographic method, sonoenteroclysis, is a promising technique for diagnosing small intestinal disorders.
  • METHODS: Forty-five consecutive patients with suspected small bowel disorder were studied.
  • All patients underwent abdominal ultrasound before and after infusion of an isotonic nonabsorbable electrolyte solution containing polyethylene glycol through a nasojejunal tube (modified Billbao Dotter tube), and images at various levels were obtained.
  • Small bowel wall thickness, luminal narrowing, intestinal dilatation, peristalsis, and extraintestinal complications were noted.
  • RESULTS: Satisfactory distention of the intestinal lumen was obtained with sequential visualization of jejunoileal loops in 34.4 +/- 18.4 min.
  • Of 45 patients, 10 showed normal small bowel on sonoenteroclysis and barium enteroclysis.
  • The remaining 35 patients showed abnormalities in the form of strictures, matted bowel loops, dilated loops, thickened folds, deformed ileocecal junction, mass lesions, etc., on sonoenteroclysis and barium enteroclysis.
  • These were diagnosed subsequently as cases of tuberculosis (n = 23), celiac disease (n = 6), adenocarcinoma (n = 2), leiomyoma (n = 2), Immunoproliferative small intestinal disease (n = 1), and segmental enteritis (n = 1).
  • CONCLUSIONS: The diagnostic accuracy of sonoenteroclysis for detecting small bowel lesions is comparable to that of barium enteroclysis.
  • This new, widely available, inexpensive, and undemanding technique can be used as an initial investigation in the evaluation of patients with small bowel disorders.
  • [MeSH-major] Intestinal Diseases / ultrasonography. Intestine, Small / ultrasonography

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16447095.001).
  • [ISSN] 0942-8925
  • [Journal-full-title] Abdominal imaging
  • [ISO-abbreviation] Abdom Imaging
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 25BB7EKE2E / Barium Sulfate; 30IQX730WE / Polyethylene Glycols
  •  go-up   go-down


82. Suarez F, Lortholary O, Hermine O, Lecuit M: Infection-associated lymphomas derived from marginal zone B cells: a model of antigen-driven lymphoproliferation. Blood; 2006 Apr 15;107(8):3034-44
MedlinePlus Health Information. consumer health - Bacterial Infections.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Infection-associated lymphomas derived from marginal zone B cells: a model of antigen-driven lymphoproliferation.
  • Non-Hodgkin lymphomas develop from nodal and extranodal lymphoid tissues.
  • A distinct subset of extranodal lymphomas arising from B cells of the marginal zone (MZ) of mucosa-associated lymphoid tissue (MALT) or spleen has been individualized.
  • Growing evidence indicates that MZ lymphomas are associated with chronic antigenic stimulation by microbial pathogens and/or autoantigens.
  • The list of microbial species associated with MZ lymphoproliferations has grown longer with molecular investigations and now comprises at least 5 distinct members: H. pylori, C. jejuni, B. burgdorferi, C. psittaci, and hepatitis C virus (HCV), which have been associated with gastric lymphoma, immunoproliferative small intestinal disease, cutaneous lymphoma, ocular lymphoma, and spleen lymphoma, respectively.
  • [MeSH-major] Antigen Presentation / immunology. Antigens, Bacterial / immunology. B-Lymphocytes / immunology. Bacterial Infections / immunology. Cell Proliferation. Lymphoma, B-Cell / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16397126.001).
  • [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 / Antigens, Bacterial
  • [Number-of-references] 162
  •  go-up   go-down


83. Helbling D, Mueller BU, Timchenko NA, Schardt J, Eyer M, Betts DR, Jotterand M, Meyer-Monard S, Fey MF, Pabst T: CBFB-SMMHC is correlated with increased calreticulin expression and suppresses the granulocytic differentiation factor CEBPA in AML with inv(16). Blood; 2005 Aug 15;106(4):1369-75
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This rearrangement fuses the CBFB and MYH11 genes, with the latter encoding the smooth muscle myosin heavy chain (SMMHC).
  • The myeloid transcription factor CCAAT/enhancer-binding protein alpha (CEBPA) is crucial for normal granulopoiesis.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Calreticulin / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Cell Differentiation. Female. Humans. Male. Middle Aged. RNA, Neoplasm / analysis. RNA, Small Interfering / pharmacology. Translocation, Genetic

  • COS Scholar Universe. author profiles.
  • 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 = 15855281.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Calreticulin; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / inv(16) fusion protein, human
  •  go-up   go-down


84. Ramadeen A, Laurent G, dos Santos CC, Hu X, Connelly KA, Holub BJ, Mangat I, Dorian P: n-3 Polyunsaturated fatty acids alter expression of fibrotic and hypertrophic genes in a dog model of atrial cardiomyopathy. Heart Rhythm; 2010 Apr;7(4):520-8
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.
  • Results were confirmed with quantitative real-time polymerase chain reaction (RT-PCR) and histology on all 36 dogs.
  • RESULTS: Microarray or quantitative RT-PCR results showed that SAVP-No PUFAs dogs had significantly increased mRNA levels of protein kinase B (Akt), epidermal growth factor (EGF), JAM3, myosin heavy chain alpha (MHCalpha), and CD99 and significantly decreased levels of Smad6 compared with CTRL dogs.
  • [MeSH-minor] Animals. Disease Models, Animal. Dogs. Fibrosis / genetics. Gene Expression / drug effects. Hypertrophy / genetics. Stress, Mechanical


85. Makino N, Toyofuku T, Takegahara N, Takamatsu H, Okuno T, Nakagawa Y, Kang S, Nojima S, Hori M, Kikutani H, Kumanogoh A: Involvement of Sema4A in the progression of experimental autoimmune myocarditis. FEBS Lett; 2008 Nov 26;582(28):3935-40
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.
  • Dendritic cells pulsed with myosin heavy chain-alpha peptides induced severe myocarditis in wild-type mice, but not in Sema4A-deficient mice.
  • In adoptive transfer experiments, CD4+ T-cells from wild-type mice induced severe myocarditis, while CD4+ T-cells from Sema4A-deficient mice exhibited considerably attenuated myocarditis.
  • [MeSH-major] Autoimmune Diseases / immunology. CD4-Positive T-Lymphocytes / immunology. Myocarditis / immunology. Semaphorins / physiology
  • [MeSH-minor] Adoptive Transfer. Animals. Cell Differentiation / genetics. Disease Models, Animal. Disease Progression. Disease Susceptibility. Lymphocyte Activation / genetics. Mice. Mice, Inbred BALB C. Mice, Knockout. Mice, SCID. Th1 Cells / immunology

  • MedlinePlus Health Information. consumer health - Autoimmune Diseases.
  • 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 = 18977352.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Sema4A protein, mouse; 0 / Semaphorins
  •  go-up   go-down


86. Meurs KM, Mealey KL: Evaluation of the flanking nucleotide sequences of sarcomeric hypertrophic cardiomyopathy substitution mutations. Mutat Res; 2008 Jul 3;642(1-2):86-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hypertrophic cardiomyopathy (HCM) is a familial myocardial disease with a prevalence of 1 in 500.
  • Within a population, examples of recurring identical disease causing mutations that appear to have arisen independently have been noted as well as those that appear to have been inherited from a common ancestor.
  • The objective of this study was to evaluate the most commonly reported HCM genes, beta myosin heavy chain (MYH7), myosin binding protein C, troponin I, troponin T, cardiac regulatory myosin light chain, cardiac essential myosin light chain, alpha tropomyosin and cardiac alpha-actin for sequence patterns surrounding the substitution mutations that may suggest a mechanism of increased mutability.

  • Genetic Alliance. consumer health - Cardiomyopathy.
  • Genetic Alliance. consumer health - Hypertrophic Cardiomyopathy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18539302.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


87. Heo SH, Lee SJ, Ryoo HM, Park JY, Cho JY: Identification of putative serum glycoprotein biomarkers for human lung adenocarcinoma by multilectin affinity chromatography and LC-MS/MS. Proteomics; 2007 Dec;7(23):4292-302
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Glycoproteins in human serum play fundamental roles in many biological processes, and also have clinical value as biomarkers for disease progression and treatment.
  • We identified several cancer-selective proteins that have been previously characterized as potential indicators of lung cancer in serum or plasma, including haptoglobin (HP), inter-alpha-trypsin inhibitor heavy chain 4 (ITI-H4), complement C3 precursor, and leucine-rich alpha-2-glycoprotein.
  • In addition, plasma kallikrein (KLKB1) and inter-alpha-trypsin inhibitor heavy chain 3 (ITI-H3) were identified as being potentially elevated in the lung cancer group, and were validated by Western blot analysis.
  • [MeSH-minor] Aged. Alpha-Globulins / analysis. Alpha-Globulins / chemistry. Blood Proteins / analysis. Blood Proteins / chemistry. Blotting, Western. Electrophoresis, Polyacrylamide Gel. Gene Expression / physiology. Humans. Lectins / chemistry. Male. Middle Aged. Peptide-N4-(N-acetyl-beta-glucosaminyl) Asparagine Amidase / chemistry. Plasma Kallikrein / analysis. Plasma Kallikrein / chemistry. Reproducibility of Results. Up-Regulation

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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 = 17963278.001).
  • [ISSN] 1615-9853
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Alpha-Globulins; 0 / Biomarkers, Tumor; 0 / Blood Proteins; 0 / Glycoproteins; 0 / Lectins; 39346-44-6 / inter-alpha-inhibitor; EC 3.4.21.34 / Plasma Kallikrein; EC 3.5.1.52 / Peptide-N4-(N-acetyl-beta-glucosaminyl) Asparagine Amidase
  •  go-up   go-down


88. Pidkovka NA, Cherepanova OA, Yoshida T, Alexander MR, Deaton RA, Thomas JA, Leitinger N, Owens GK: Oxidized phospholipids induce phenotypic switching of vascular smooth muscle cells in vivo and in vitro. Circ Res; 2007 Oct 12;101(8):792-801
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.
  • Atherosclerosis is a vascular disease characterized by lipid deposition and inflammation within the arterial wall.
  • Phenotypic switching of smooth muscle cells (SMCs) plays a critical role in the development, progression, and end-stage clinical consequences of atherosclerosis, yet little is known regarding the effects of specific oxPLs on SMC phenotype.
  • Results showed that POVPC and PGPC induced profound suppression of smooth muscle (SM) alpha-actin and SM myosin heavy chain expression while simultaneously increasing expression of MCP-1, MCP-3, and cytolysin.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Circ Res. 2007 Oct 12;101(8):750-1 [17932331.001]
  • (PMID = 17704209.001).
  • [ISSN] 1524-4571
  • [Journal-full-title] Circulation research
  • [ISO-abbreviation] Circ. Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / P01HL19242; United States / NHLBI NIH HHS / HL / R01HL084422-01; United States / NHLBI NIH HHS / HL / R01HL38854; United States / NHLBI NIH HHS / HL / R37HL57353
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GKLF protein; 0 / Kruppel-Like Transcription Factors; 0 / Phospholipids
  •  go-up   go-down


89. Lecuit M, Lortholary O: [Immunoproliferative small intestinal disease associated with Campylobacter jejuni]. Med Mal Infect; 2005 Jun;35 Suppl 2:S56-8
MedlinePlus Health Information. consumer health - Campylobacter Infections.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Immunoproliferative small intestinal disease associated with Campylobacter jejuni].
  • [Transliterated title] Maladie immunoproliférative de l'intestin grêle associée à Campylobacter jejuni.
  • [MeSH-major] Campylobacter Infections / complications. Intestinal Diseases / microbiology. Lymphoma, B-Cell, Marginal Zone / microbiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15978389.001).
  • [ISSN] 0399-077X
  • [Journal-full-title] Médecine et maladies infectieuses
  • [ISO-abbreviation] Med Mal Infect
  • [Language] fre
  • [Publication-type] Journal Article
  • [Publication-country] France
  •  go-up   go-down


90. Lankarani KB, Masoompour SM, Masoompour MB, Malekzadeh R, Tabei SZ, Haghshenas M: Changing epidemiology of IPSID in Southern Iran. Gut; 2005 Feb;54(2):311-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Changing epidemiology of IPSID in Southern Iran.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / epidemiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 1968 Dec 20;162(3860):1396-7 [4177362.001]
  • [Cites] Gut. 1970 Aug;11(8):673-8 [4919259.001]
  • [Cites] Cancer. 1971 Apr;27(4):965-77 [5574084.001]
  • [Cites] IARC Sci Publ. 1991;(95):126-58 [1894318.001]
  • [Cites] Am J Dig Dis. 1977 Oct;22(10):866-73 [411371.001]
  • [Cites] N Engl J Med. 1983 Jun 9;308(23):1401-5 [6405275.001]
  • [Cites] Bull World Health Organ. 1976;54(6):615-24 [829415.001]
  • (PMID = 15647204.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1774824
  •  go-up   go-down


91. Xu SQ, Fang F, Zhou H: [Immunoproliferative small intestinal disease: a case report and literature review]. Zhongguo Dang Dai Er Ke Za Zhi; 2007 Aug;9(4):389-91

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Immunoproliferative small intestinal disease: a case report and literature review].
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17706052.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Immunoglobulin A
  •  go-up   go-down






Advertisement