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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
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  • [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.

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  • [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
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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
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  • 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

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  • (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
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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
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  • 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

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

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  • [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.

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  • [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
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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
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  • [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

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  • (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
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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
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  • [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

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

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  • 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

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  • [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
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8. 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
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  • [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

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  • [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
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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
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  • 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.

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  • (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
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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
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  • [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

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

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  • (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
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12. 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
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  • [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

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  • (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
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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

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  • [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

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  • (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
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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

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

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  • 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.

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  • (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
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16. Zhou H, Hickford JG, Fang Q: Polymorphism of the IGHA gene in sheep. Immunogenetics; 2005 Jul;57(6):453-7
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  • 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

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  • [Cites] Vet Immunol Immunopathol. 1999 Dec 15;72(1-2):143-55 [10614504.001]
  • [Cites] Mol Biochem Parasitol. 2003 Aug 11;130(1):23-9 [14550893.001]
  • [Cites] Immunogenetics. 2004 Jul;56(4):254-60 [15241634.001]
  • [Cites] Annu Rev Microbiol. 1983;37:603-22 [6416146.001]
  • [Cites] Cell. 1984 Mar;36(3):681-8 [6421489.001]
  • [Cites] Immunology. 2001 Aug;103(4):441-8 [11529934.001]
  • [Cites] Immunogenetics. 1998 Oct;48(5):359-62 [9745016.001]
  • [Cites] Immunology. 1997 May;91(1):1-6 [9203958.001]
  • [Cites] Vet Immunol Immunopathol. 1999 Dec 15;72(1-2):213-8 [10614511.001]
  • [Cites] Dev Comp Immunol. 2005;29(3):185-203 [15572068.001]
  • [Cites] Nucleic Acids Res. 1984 Feb 10;12(3):1303-11 [6322103.001]
  • [Cites] Immunogenetics. 2002 Mar;53(12):1033-8 [11904680.001]
  • [Cites] J Immunol. 1994 Jun 1;152(11):5299-304 [8189047.001]
  • [Cites] Immunology. 2004 Oct;113(2):175-7 [15379977.001]
  • [Cites] J Immunol. 1995 Apr 15;154(8):3836-42 [7706723.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Dec;78(12):7684-8 [6801659.001]
  • [Cites] Mol Biol Evol. 2002 Jul;19(7):1093-9 [12082128.001]
  • [Cites] Anal Biochem. 1991 Jul;196(1):80-3 [1716076.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D593-7 [15608269.001]
  • [Cites] APMIS. 1996 May;104(5):321-38 [8703438.001]
  • [Cites] Infect Immun. 2003 Mar;71(3):1462-9 [12595464.001]
  • [Cites] J Mol Biol. 2004 May 14;338(5):921-41 [15111057.001]
  • (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
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17. 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.

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  • (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
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18. 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
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  • 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

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  • (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
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19. 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
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  • 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

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  • (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
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20. 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
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  • [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.

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  • [Cites] Clin Cancer Res. 2001 Apr;7(4):896-900 [11309339.001]
  • [Cites] Virchows Arch. 1994;424(3):257-66 [7514477.001]
  • [Cites] Lab Invest. 1983 Aug;49(2):140-7 [6348406.001]
  • [Cites] FASEB J. 1990 Feb 1;4(2):148-60 [2404817.001]
  • [Cites] Oncology. 2002;62(4):318-26 [12138239.001]
  • [Cites] Cancer. 1990 Dec 15;66(12):2583-8 [2249199.001]
  • [Cites] Anticancer Res. 2001 Jan-Feb;21(1B):509-12 [11299796.001]
  • [Cites] Cancer. 2003 Jul 15;98(2):413-23 [12872364.001]
  • [Cites] Acta Otolaryngol. 1991;111(2):437-43 [2068933.001]
  • [Cites] J Oral Pathol Med. 1989 Sep;18(8):432-7 [2607465.001]
  • [Cites] Br J Cancer. 1999 Nov;81(6):1071-9 [10576667.001]
  • [Cites] Anticancer Res. 1998 Nov-Dec;18(6B):4757-64 [9891553.001]
  • [Cites] Cancer. 2001 Mar 15;91(6):1129-41 [11267958.001]
  • [Cites] Hum Pathol. 1998 May;29(5):447-54 [9596267.001]
  • [Cites] Acta Radiol Ther Phys Biol. 1973 Feb;12(1):1-8 [4725642.001]
  • [Cites] Pathol Int. 2004 Sep;54(9):688-92 [15363037.001]
  • [Cites] Eur J Biochem. 1989 Apr 1;180(3):487-502 [2653817.001]
  • [Cites] Cancer. 1999 Jun 1;85(11):2315-21 [10357399.001]
  • [Cites] Pathol Int. 1995 May;45(5):327-34 [7647928.001]
  • [Cites] Cancer Res. 1981 Dec;41(12 Pt 1):5076-81 [7030483.001]
  • [Cites] Histopathology. 1999 Apr;34(4):305-9 [10231397.001]
  • [Cites] Br J Dermatol. 1997 Mar;136(3):331-6 [9115910.001]
  • [Cites] Laryngorhinootologie. 1994 Dec;73(12):637-41 [7840826.001]
  • [Cites] Curr Opin Otolaryngol Head Neck Surg. 2005 Apr;13(2):101-4 [15761284.001]
  • [Cites] Int J Oncol. 2001 May;18(5):1045-51 [11295055.001]
  • (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
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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
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  • [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

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  • (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
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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
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  • 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.

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  • [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
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23. Salem PA, Estephan FF: Immunoproliferative small intestinal disease: current concepts. Cancer J; 2005 Sep-Oct;11(5):374-82
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  • [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

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  • (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
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24. 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

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  • (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
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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
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  • [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

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  • (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
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26. Yu X, Mollan TL, Butler A, Gow AJ, Olson JS, Weiss MJ: Analysis of human alpha globin gene mutations that impair binding to the alpha hemoglobin stabilizing protein. Blood; 2009 Jun 4;113(23):5961-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of human alpha globin gene mutations that impair binding to the alpha hemoglobin stabilizing protein.
  • Alpha hemoglobin stabilizing protein (AHSP) reversibly binds nascent alpha globin to maintain its native structure and facilitate its incorporation into hemoglobin A.
  • Previous studies indicate that some naturally occurring human alpha globin mutations may destabilize the protein by inhibiting its interactions with AHSP.
  • We analyzed 6 human alpha globin variants with altered AHSP contact surfaces.
  • Alpha globin amino acid substitutions H103Y, H103R, F117S, and P119S impaired interactions with both AHSP and beta globin.
  • By contrast, K99E and K99N alpha globins bind beta globin normally but exhibit attenuated binding to AHSP.
  • In Escherichia coli and erythroid cells, alpha globin K99E stability is rescued on coexpression with AHSP mutants in which binding to the abnormal globin chain is restored.
  • Our results better define the biochemical properties of some alpha globin variants and support the hypothesis that AHSP promotes alpha globin chain stability during human erythropoiesis.

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  • [Cites] J Biol Chem. 2002 Apr 19;277(16):13415-20 [11827978.001]
  • [Cites] Biochim Biophys Acta. 2008 Oct;1784(10):1462-70 [18267132.001]
  • [Cites] Hemoglobin. 2002 May;26(2):175-9 [12144061.001]
  • [Cites] J Biol Chem. 2002 Oct 25;277(43):40602-9 [12192002.001]
  • [Cites] Hemoglobin. 2002 Aug;26(3):255-60 [12403490.001]
  • [Cites] Hemoglobin. 2003 Feb;27(1):45-7 [12603094.001]
  • [Cites] Arch Biochem Biophys. 2003 May 1;413(1):99-106 [12706346.001]
  • [Cites] Hemoglobin. 2003 May;27(2):123-7 [12779275.001]
  • [Cites] Hemoglobin. 2004 Feb;28(1):59-63 [15008266.001]
  • [Cites] Blood. 2004 May 1;103(9):3296-9 [14715623.001]
  • [Cites] J Biol Chem. 1976 Dec 25;251(24):7871-9 [12181.001]
  • [Cites] Biochim Biophys Acta. 1979 Jun 19;578(2):534-40 [486536.001]
  • [Cites] Hemoglobin. 1984;8(2):169-81 [6547932.001]
  • [Cites] J Mol Biol. 1985 Mar 20;182(2):331-40 [3923205.001]
  • [Cites] J Biol Chem. 1986 Nov 15;261(32):15327-33 [3771577.001]
  • [Cites] J Biol Chem. 1987 May 5;262(13):5951-6 [3571243.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8521-5 [2236062.001]
  • [Cites] Nature. 1992 Mar 19;356(6366):258-60 [1552945.001]
  • [Cites] Hemoglobin. 1992;16(1-2):11-7 [1634357.001]
  • [Cites] Hemoglobin. 1992;16(4):275-9 [1517104.001]
  • [Cites] Hemoglobin. 1992;16(5):435-9 [1428950.001]
  • [Cites] Methods Enzymol. 1994;231:347-64 [8041262.001]
  • [Cites] Immunity. 1999 Sep;11(3):299-308 [10514008.001]
  • [Cites] J Clin Invest. 2004 Nov;114(10):1457-66 [15545996.001]
  • [Cites] Cell. 2004 Nov 24;119(5):629-40 [15550245.001]
  • [Cites] Nature. 2005 Jun 2;435(7042):697-701 [15931225.001]
  • [Cites] Hemoglobin. 2005;29(4):263-8 [16370486.001]
  • [Cites] Br J Haematol. 2006 Feb;132(3):370-3 [16409302.001]
  • [Cites] Protein Eng Des Sel. 2006 Mar;19(3):91-7 [16390839.001]
  • [Cites] J Biol Chem. 2006 Oct 27;281(43):32611-8 [16901899.001]
  • [Cites] Blood Cells Mol Dis. 2006 Nov-Dec;37(3):173-9 [17052927.001]
  • [Cites] J Biol Inorg Chem. 2007 Jan;12(1):101-17 [16972088.001]
  • [Cites] Hemoglobin. 2007;31(2):179-82 [17486500.001]
  • [Cites] J Clin Invest. 2007 Jul;117(7):1856-65 [17607360.001]
  • [Cites] Ann Hematol. 2007 Sep;86(9):665-9 [17589844.001]
  • [Cites] Haematologica. 2008 Jan;93(1):141-2 [18166800.001]
  • [Cites] Am J Hematol. 2008 Feb;83(2):103-8 [17874450.001]
  • [Cites] Exp Hematol. 2008 Mar;36(3):265-72 [18179859.001]
  • [Cites] Nature. 2002 Jun 13;417(6890):758-63 [12066189.001]
  • (PMID = 19349619.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R56 DK061692; United States / NIGMS NIH HHS / GM / T32 GM008362; United States / NHLBI NIH HHS / HL / HL47020; United States / NIEHS NIH HHS / ES / P30 ES005022; United States / NIGMS NIH HHS / GM / GM008362; United States / NIGMS NIH HHS / GM / GM35649; United States / NIDDK NIH HHS / DK / DK061692; United States / NIGMS NIH HHS / GM / R01 GM035649; United States / NIDDK NIH HHS / DK / R01 DK061692; United States / NHLBI NIH HHS / HL / R01 HL087427; United States / NHLBI NIH HHS / HL / HL087427; United States / NHLBI NIH HHS / HL / R01 HL047020
  • [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 / AHSP protein, human; 0 / Blood Proteins; 0 / Molecular Chaperones; 0 / alpha-Globins; 0 / beta-Globins; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC2700329
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27. Anwari K, Poggio S, Perry A, Gatsos X, Ramarathinam SH, Williamson NA, Noinaj N, Buchanan S, Gabriel K, Purcell AW, Jacobs-Wagner C, Lithgow T: A modular BAM complex in the outer membrane of the alpha-proteobacterium Caulobacter crescentus. PLoS One; 2010 Jan 08;5(1):e8619
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A modular BAM complex in the outer membrane of the alpha-proteobacterium Caulobacter crescentus.
  • Mitochondria are organelles derived from an intracellular alpha-proteobacterium.
  • Caulobacter crescentus is an alpha-proteobacterium, and the BAM (beta-barrel assembly machinery) complex was purified and characterized from this model organism.

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  • [Cites] Microbiol Mol Biol Rev. 2000 Dec;64(4):786-820 [11104819.001]
  • [Cites] J Biol Chem. 2004 Apr 30;279(18):18188-94 [14978039.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Mar 27;98(7):4136-41 [11259647.001]
  • [Cites] Bioinformatics. 2001 Apr;17(4):377-8 [11301311.001]
  • [Cites] J Biol Chem. 2002 Apr 19;277(16):14274-80 [11830585.001]
  • [Cites] Science. 2003 Jan 10;299(5604):262-5 [12522254.001]
  • [Cites] EMBO J. 2003 Apr 15;22(8):1780-9 [12682011.001]
  • [Cites] Dev Cell. 2004 Jul;7(1):61-71 [15239954.001]
  • [Cites] J Cell Biol. 1966 Mar;28(3):423-36 [5960805.001]
  • [Cites] J Biochem. 1981 Apr;89(4):1059-66 [7019204.001]
  • [Cites] Anal Biochem. 1991 Dec;199(2):223-31 [1812789.001]
  • [Cites] Nature. 1998 Mar 5;392(6671):37-41 [9510246.001]
  • [Cites] Cell. 1998 Apr 3;93(1):17-20 [9546387.001]
  • [Cites] J Bacteriol. 1999 Feb;181(4):1099-109 [9973334.001]
  • [Cites] Science. 1999 Mar 5;283(5407):1476-81 [10066161.001]
  • [Cites] Nat Struct Mol Biol. 2004 Nov;11(11):1044-8 [15523480.001]
  • [Cites] Bacteriol Rev. 1964 Sep;28:231-95 [14220656.001]
  • [Cites] J Infect Dis. 2005 Mar 15;191(6):939-48 [15717270.001]
  • [Cites] J Bacteriol. 2005 Apr;187(7):2286-96 [15774871.001]
  • [Cites] Cell. 2005 Apr 22;121(2):235-45 [15851030.001]
  • [Cites] Infect Immun. 2005 Sep;73(9):6075-84 [16113328.001]
  • [Cites] J Bacteriol. 2005 Oct;187(20):6874-82 [16199556.001]
  • [Cites] J Biol Chem. 2005 Oct 14;280(41):34409-19 [16079137.001]
  • [Cites] Mol Microbiol. 2005 Dec;58(5):1216-25 [16313611.001]
  • [Cites] J Bacteriol. 2005 Dec;187(24):8300-11 [16321934.001]
  • [Cites] Biochemistry. 2006 Feb 21;45(7):2122-8 [16475801.001]
  • [Cites] J Mol Biol. 2006 May 12;358(4):1010-22 [16566938.001]
  • [Cites] Mol Microbiol. 2006 Jul;61(1):151-64 [16824102.001]
  • [Cites] J Biol Chem. 2006 Aug 11;281(32):22819-26 [16760475.001]
  • [Cites] Infect Immun. 2007 Jan;75(1):358-70 [17060472.001]
  • [Cites] J Cell Biol. 2007 Jan 1;176(1):77-88 [17190789.001]
  • [Cites] Mol Microbiol. 2007 Feb;63(4):1008-25 [17233825.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 10;104(15):6400-5 [17404237.001]
  • [Cites] Curr Opin Struct Biol. 2007 Apr;17(2):260-7 [17398087.001]
  • [Cites] Mol Microbiol. 2007 May;64(4):938-52 [17501919.001]
  • [Cites] Science. 2007 Aug 17;317(5840):961-4 [17702946.001]
  • [Cites] J Biol Chem. 2008 Jan 4;283(1):120-7 [17974559.001]
  • [Cites] J Mol Biol. 2008 Feb 22;376(3):671-80 [18177669.001]
  • [Cites] J Mol Biol. 2008 Feb 22;376(3):694-704 [18187149.001]
  • [Cites] J Bacteriol. 2008 Mar;190(5):1507-17 [18165306.001]
  • [Cites] Microbiology. 2008 Mar;154(Pt 3):979-88 [18310044.001]
  • [Cites] Mol Microbiol. 2008 Jun;68(5):1216-27 [18430136.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Jul 29;105(30):10348-53 [18647830.001]
  • [Cites] Mol Microbiol. 2008 Nov;70(3):634-51 [18786147.001]
  • [Cites] FEMS Microbiol Rev. 2008 Nov;32(6):995-1009 [18759741.001]
  • [Cites] Structure. 2008 Dec 10;16(12):1873-81 [19081063.001]
  • [Cites] Nat Rev Microbiol. 2009 Mar;7(3):206-14 [19182809.001]
  • [Cites] Bioinformatics. 2009 May 1;25(9):1189-91 [19151095.001]
  • [Cites] FEBS Lett. 2009 May 6;583(9):1475-80 [19345216.001]
  • [Cites] J Biochem. 2009 Aug;146(2):219-29 [19364805.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Sep 15;106(37):15791-5 [19717453.001]
  • [Cites] J Bacteriol. 2009 Nov;191(22):7074-85 [19767435.001]
  • [Cites] Microbiology. 2009 Dec;155(Pt 12):3982-91 [19815580.001]
  • [Cites] J Am Chem Soc. 2007 Apr 18;129(15):4800-7 [17375930.001]
  • [Cites] J Bacteriol. 2003 Oct;185(20):6112-8 [14526023.001]
  • [Cites] Arch Biochem Biophys. 2003 Dec 1;420(1):130-41 [14622983.001]
  • [Cites] J Biol Chem. 2003 Dec 5;278(49):48520-3 [14570913.001]
  • [Cites] Nature. 2003 Dec 18;426(6968):862-6 [14685243.001]
  • [Cites] J Cell Biol. 2004 Jan 5;164(1):19-24 [14699090.001]
  • [Cites] Mol Microbiol. 2004 Feb;51(4):1027-37 [14763978.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):12396-405 [14722057.001]
  • [Cites] J Immunol. 2001 Jan 15;166(2):1016-27 [11145681.001]
  • (PMID = 20062535.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM076698; United States / NIGMS NIH HHS / GM / GM065835; United States / Intramural NIH HHS / / ; United States / NIGMS NIH HHS / GM / R01 GM065835; United States / NIGMS NIH HHS / GM / GM076698
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Outer Membrane Proteins; 0 / DNA Primers
  • [Other-IDs] NLM/ PMC2797634
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28. Ye Y, Wu Q, Yao L, Dong X, Wu K, Zhang J: A comparison of polymerase chain reaction and international organization for standardization methods for determination of Enterobacter sakazakii contamination of infant formulas from Chinese mainland markets. Foodborne Pathog Dis; 2009 Dec;6(10):1229-34
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  • [Title] A comparison of polymerase chain reaction and international organization for standardization methods for determination of Enterobacter sakazakii contamination of infant formulas from Chinese mainland markets.
  • To provide efficient options and direction for detecting E. sakazakii in infant formulas, evaluation of different polymerase chain reaction (PCR) assays targeting the 16S-23S rDNA internal transcribed spacer (ITS), the ompA gene, and the alpha-1,4-glucosidase gene (gluA) of this organism, were compared to the International Organization for Standardization (ISO) method for detecting E. sakazakii in the 243 commercial infant formula samples.
  • [MeSH-major] Cronobacter sakazakii / isolation & purification. Infant Food / microbiology. Infant Formula. Polymerase Chain Reaction / methods
  • [MeSH-minor] Animals. Bacterial Outer Membrane Proteins / genetics. Bacterial Outer Membrane Proteins / metabolism. China. DNA, Bacterial / chemistry. DNA, Ribosomal Spacer / chemistry. DNA, Ribosomal Spacer / genetics. DNA, Ribosomal Spacer / metabolism. Food Microbiology. Humans. Infant. Limit of Detection. Reagent Kits, Diagnostic. Sequence Analysis, DNA. Time Factors. alpha-Glucosidases / genetics. alpha-Glucosidases / metabolism

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  • (PMID = 19743923.001).
  • [ISSN] 1556-7125
  • [Journal-full-title] Foodborne pathogens and disease
  • [ISO-abbreviation] Foodborne Pathog. Dis.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Outer Membrane Proteins; 0 / DNA, Bacterial; 0 / DNA, Ribosomal Spacer; 0 / Reagent Kits, Diagnostic; 149024-69-1 / OMPA outer membrane proteins; EC 3.2.1.20 / alpha-Glucosidases
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29. Yuan GJ, Gong ZJ, Sun XM, Zheng SH, Li X: Tea polyphenols inhibit expressions of iNOS and TNF-alpha and prevent lipopolysaccharide-induced liver injury in rats. Hepatobiliary Pancreat Dis Int; 2006 May;5(2):262-7
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  • [Title] Tea polyphenols inhibit expressions of iNOS and TNF-alpha and prevent lipopolysaccharide-induced liver injury in rats.
  • Serum tumor necrosis factor-alpha (TNF-alpha) levels and liver malondialdehyde (MDA) contents were determined.
  • Inducible nitric oxide synthase (iNOS) protein and TNF-alpha, iNOS and endothelial nitric oxide synthase (eNOS) mRNA expressions in the liver were detected by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR), respectively.
  • These responses were associated with increased serum TNF-alpha levels, induced iNOS protein, expressions of TNF-alpha, iNOS mRNA in the liver and elevated lipid peroxidation at 90 minutes or 6 hours after LPS injection.
  • Pretreatment with tea polyphenols attenuated LPS-induced liver injury, and blunted the rises of serum TNF-alpha levels and lipid peroxidation and the induction of expressions of TNF-alpha, iNOS in the liver.
  • CONCLUSION: Tea polyphenols prevent LPS-induced liver injury, and the mechanisms may involve the reduction of serum TNF-alpha levels and lipid peroxidation and the suppression of TNF-alpha, iNOS expressions in the liver.
  • [MeSH-major] Flavonoids / pharmacology. Liver / drug effects. Liver / metabolism. Liver Diseases / pathology. Nitric Oxide Synthase Type II / metabolism. Phenols / pharmacology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Analysis of Variance. Animals. Base Sequence. Biopsy, Needle. Disease Models, Animal. Drug-Induced Liver Injury. Immunohistochemistry. Lipopolysaccharides. Liver Function Tests. Male. Molecular Sequence Data. Polyphenols. Probability. RNA, Messenger / analysis. Random Allocation. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity. Tissue Culture Techniques

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  • (PMID = 16698588.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Lipopolysaccharides; 0 / Phenols; 0 / Polyphenols; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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30. Shaye OS, Levine AM: Marginal zone lymphoma. J Natl Compr Canc Netw; 2006 Mar;4(3):311-8
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  • [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

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  • (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
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31. 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
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  • [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

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  • [Cites] Int J Pancreatol. 2001;29(1):59-62 [11558634.001]
  • [Cites] Acta Chir Scand. 1981;147(4):303-4 [6976669.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2006 Sep;18(9):1029-38 [16894320.001]
  • [Cites] Ann Surg. 1990 Apr;211(4):447-58 [2322039.001]
  • [Cites] Cancer. 1977 May;39(5):2081-101 [404026.001]
  • [Cites] Pancreas. 2002 Apr;24(3):258-63 [11893933.001]
  • [Cites] Mayo Clin Proc. 1994 Aug;69(8):736-40 [8035627.001]
  • [Cites] Semin Oncol. 2003 Aug;30(4):448-56 [12939713.001]
  • [Cites] Curr Opin Hematol. 2005 Jul;12(4):259-65 [15928481.001]
  • [Cites] Ann Surg Oncol. 2002 Nov;9(9):847-54 [12417505.001]
  • [Cites] Surg Today. 2004;34(8):701-5 [15290403.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2274-80 [15542584.001]
  • [Cites] Am J Gastroenterol. 2001 Sep;96(9):2769-74 [11569710.001]
  • [Cites] Am J Surg. 1990 Mar;159(3):282-6 [2305934.001]
  • [Cites] J Am Coll Surg. 2003 Dec;197(6):937-42 [14644281.001]
  • [Cites] Hepatogastroenterology. 1999 May-Jun;46(27):1953-8 [10430376.001]
  • [Cites] Ann Surg. 1993 May;217(5):430-5; discussion 435-8 [8098202.001]
  • (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
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32. Coelho A, Picanço I, Seuanes F, Seixas MT, Faustino P: Novel large deletions in the human alpha-globin gene cluster: Clarifying the HS-40 long-range regulatory role in the native chromosome environment. Blood Cells Mol Dis; 2010 Aug 15;45(2):147-53
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  • [Title] Novel large deletions in the human alpha-globin gene cluster: Clarifying the HS-40 long-range regulatory role in the native chromosome environment.
  • Concerning the human alpha-globin gene cluster (located at chromosome region 16p13.3), four upstream highly conserved elements known as multispecies conserved sequences (MCS-R1-4) or DNase I hypersensitive sites (HSs) are implicated in the long-range regulation of downstream gene expression.
  • In this study, Multiplex Ligation-dependent Probe Amplification was used to screen for deletions in the telomeric region of the short arm of chromosome 16, in an attempt to explain the alpha-thalassemia or the HbH disease present in a group of Portuguese patients.
  • We report four novel and five uncommon deletions that remove the alpha-globin distal regulatory elements and/or the complete alpha-globin gene cluster.
  • Interestingly, one of them occurred de novo and removes all HSs except HS-10, while other eliminates only the HS-40 site, the latter being replaced by the insertion of a 39 nucleotide orphan sequence.
  • Our results demonstrate that HS-10 alone does not significantly enhance the alpha-globin gene expression.
  • The absence of HS-40 in homozygosity, found in a patient with Hb H disease, strongly downregulates the expression of alpha-globin genes but it is not associated with a complete absence of alpha-globin chain production.
  • [MeSH-major] Hemoglobin H / genetics. Regulatory Elements, Transcriptional / genetics. Sequence Deletion / genetics. alpha-Globins / genetics. alpha-Thalassemia / genetics

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20580289.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / alpha-Globins; 9034-79-1 / Hemoglobin H
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33. Pastor DM, Irby RB, Poritz LS: Tumor necrosis factor alpha induces p53 up-regulated modulator of apoptosis expression in colorectal cancer cell lines. Dis Colon Rectum; 2010 Mar;53(3):257-63
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  • [Title] Tumor necrosis factor alpha induces p53 up-regulated modulator of apoptosis expression in colorectal cancer cell lines.
  • PURPOSE: Inflammatory bowel disease (IBD)-associated colorectal carcinogenesis involves dysregulation of multiple cellular pathways, including p53 signaling and cytokine action.
  • The purpose of the current study was to evaluate the effects of tumor necrosis factor alpha (TNF-alpha) on p53 and p53 up-regulated modulator of apoptosis (PUMA), a downstream effector of p53 in the apoptotic pathway in colorectal cancer cells.
  • METHODS: The cell lines HT29 (which express mutant p53) and HCT116 (which express wild-type p53) were treated with TNF-alpha (0, 50, 100, or 500 ng/mL) for 1, 12, 24, or 48 hours.
  • Changes in p53 and PUMA mRNA expression were determined by quantitative real time polymerase chain reaction.
  • RESULTS: Nuclear p53 expression was increased in TNF-alpha-treated HT29 cells; in contrast, expression was decreased or minimally changed in TNF-alpha-treated HCT116 cells, as determined by immunoblot and immunofluorescence.
  • CONCLUSIONS: TNF-alpha increased nuclear p53 expression in HT29 cells, which express p53 mutation, but not in HCT116 cells, which are wild type for p53.
  • In addition, TNF-alpha markedly up-regulated PUMA mRNA levels in HT29 cells.
  • Our findings suggest that TNF-alpha may be a factor in carcinogenesis in IBD in cells carrying a p53 mutation.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis Regulatory Proteins / metabolism. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Analysis of Variance. Cell Line, Tumor. Fluorescent Antibody Technique. Humans. Immunoblotting. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation

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  • (PMID = 20173470.001).
  • [ISSN] 1530-0358
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53
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34. Parish ST, Wu JE, Effros RB: Modulation of T lymphocyte replicative senescence via TNF-{alpha} inhibition: role of caspase-3. J Immunol; 2009 Apr 1;182(7):4237-43
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  • [Title] Modulation of T lymphocyte replicative senescence via TNF-{alpha} inhibition: role of caspase-3.
  • Expanded populations of CD8(+) T lymphocytes lacking CD28 expression are associated with a variety of deleterious clinical outcomes, including early mortality in the elderly, more rapid progression to AIDS, cardiovascular disease, and enhanced tumor cell growth.
  • In cell culture, irreversible loss of CD28 expression correlates with increased production of TNF-alpha as CD8(+) T cells are driven to the nonproliferative end stage of replicative senescence by multiple rounds of Ag-driven cell division.
  • Interestingly, in patients with rheumatoid arthritis, inhibition or neutralization of TNF-alpha reduces the proportion of T cells lacking CD28 in the disease joints, consistent with studies showing a direct involvement of this cytokine in CD28 gene transcription.
  • Here, we show that modulation of TNF-alpha levels in long-term cultures of human CD8(+) T lymphocytes, by chronic exposure either to a neutralizing Ab or to an inhibitor of the TNF-alpha receptor-1, increases proliferative potential, delays loss of CD28 expression, retards cytokine profile changes, and enhances telomerase activity.
  • We also show that constitutive caspase-3, one of the downstream effectors of TNF-alphaR1 binding, increases in parallel with the loss of CD28 in long-term cultures, but this effect is blunted in the presence of the TNF-alpha inhibitors.
  • These findings help elucidate the complex nature of CD28 gene regulation, and may ultimately lead to novel therapeutic approaches for diseases associated with increased proportions of CD28(-) T lymphocytes.

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  • [Cites] Mech Ageing Dev. 2000 Dec 20;121(1-3):77-88 [11164462.001]
  • [Cites] Cancer Immunol Immunother. 2003 Oct;52(10):599-607 [12827303.001]
  • [Cites] Exp Gerontol. 2003 Oct;38(10):1109-18 [14580864.001]
  • [Cites] Cell Biol Int. 2003;27(12):959-64 [14642527.001]
  • [Cites] Exp Gerontol. 2004 Apr;39(4):517-24 [15050285.001]
  • [Cites] Trends Mol Med. 2004 Mar;10(3):119-24 [15102354.001]
  • [Cites] Exp Gerontol. 2004 Jun;39(6):885-90 [15217682.001]
  • [Cites] J Biol Chem. 2004 Jul 9;279(28):29130-8 [15128741.001]
  • [Cites] Science. 1989 Apr 21;244(4902):339-43 [2540528.001]
  • [Cites] Exp Gerontol. 1989;24(3):177-87 [2786475.001]
  • [Cites] J Immunol. 1990 Mar 1;144(5):1646-53 [2155264.001]
  • [Cites] Science. 1991 Jan 18;251(4991):313-6 [1846244.001]
  • [Cites] J Biol Chem. 1991 Aug 5;266(22):14179-82 [1650350.001]
  • [Cites] Lymphokine Cytokine Res. 1991 Oct;10(5):347-51 [1768737.001]
  • [Cites] J Exp Med. 1994 Feb 1;179(2):609-18 [8294871.001]
  • [Cites] Dig Dis Sci. 1994 Sep;39(9):1900-8 [8082496.001]
  • [Cites] Clin Exp Immunol. 1995 Jun;100(3):425-33 [7539725.001]
  • [Cites] Scand J Immunol. 1996 Jan;43(1):88-93 [8560201.001]
  • [Cites] J Clin Invest. 1996 May 1;97(9):2027-37 [8621791.001]
  • [Cites] Annu Rev Immunol. 1996;14:233-58 [8717514.001]
  • [Cites] AIDS. 1996 Jul;10(8):F17-22 [8828735.001]
  • [Cites] Mech Ageing Dev. 1997 Feb;93(1-3):87-94 [9089573.001]
  • [Cites] Exp Gerontol. 1994 Nov-Dec;29(6):601-9 [9435913.001]
  • [Cites] J Biol Chem. 1998 Apr 3;273(14):8119-29 [9525915.001]
  • [Cites] Immunology. 1998 May;94(1):41-7 [9708185.001]
  • [Cites] Mech Ageing Dev. 1998 May 15;102(2-3):199-209 [9720652.001]
  • [Cites] Clin Exp Immunol. 1998 Oct;114(1):113-8 [9764612.001]
  • [Cites] Immunol Rev. 1998 Oct;165:287-300 [9850868.001]
  • [Cites] Annu Rev Immunol. 1999;17:331-67 [10358762.001]
  • [Cites] AIDS. 1999 Jun 18;13(9):1029-33 [10397532.001]
  • [Cites] Exp Gerontol. 1999 Aug;34(5):633-44 [10530789.001]
  • [Cites] Exp Cell Res. 1965 Mar;37:614-36 [14315085.001]
  • [Cites] J Immunol. 2004 Nov 15;173(10):6303-11 [15528369.001]
  • [Cites] Immunol Rev. 2005 Jun;205:147-57 [15882351.001]
  • [Cites] Immunol Rev. 2005 Jun;205:158-69 [15882352.001]
  • [Cites] Arthritis Rheum. 2005 Oct;52(10):2996-3003 [16200579.001]
  • [Cites] J Immunol. 2006 Feb 15;176(4):2645-53 [16456027.001]
  • [Cites] Exp Gerontol. 2007 May;42(5):416-20 [17182206.001]
  • [Cites] J Immunol. 2008 Nov 15;181(10):7400-6 [18981163.001]
  • [Cites] Blood. 2001 Nov 1;98(9):2817-27 [11675356.001]
  • [Cites] J Virol. 2001 Dec;75(24):12182-7 [11711609.001]
  • [Cites] Exp Gerontol. 2002 Jan-Mar;37(2-3):293-9 [11772515.001]
  • [Cites] J Immunol. 2002 Jun 1;168(11):5893-9 [12023394.001]
  • [Cites] Cancer Immunol Immunother. 2002 Nov;51(9):499-504 [12357321.001]
  • [Cites] Clin Immunol. 2002 Nov;105(2):117-25 [12482386.001]
  • [Cites] Cell. 2003 Jul 25;114(2):181-90 [12887920.001]
  • [Cites] J Immunol. 2001 Sep 15;167(6):3231-8 [11544310.001]
  • (PMID = 19299722.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01 AG023720; United States / NIAID NIH HHS / AI / R01 AI060362; United States / NIA NIH HHS / AG / AG023720; United States / NIAID NIH HHS / AI / AI060362
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD28; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; EC 2.7.7.49 / Telomerase; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS509843; NLM/ PMC3773494
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35. Li L, Chen SH, Zhang Y, Yu CH, Li SD, Li YM: Is the hypoxia-inducible factor-1 alpha mRNA expression activated by ethanol-induced injury, the mechanism underlying alcoholic liver disease? Hepatobiliary Pancreat Dis Int; 2006 Nov;5(4):560-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is the hypoxia-inducible factor-1 alpha mRNA expression activated by ethanol-induced injury, the mechanism underlying alcoholic liver disease?
  • BACKGROUND: Excessive alcohol consumption can result in multiple organ injury, of which alcoholic liver disease (ALD) is the most common.
  • With economic development and improvement of living standards, the incidence of diseases caused by alcohol abuse has been increasing in China, although its pathogenesis remains obscure.
  • RESULTS: When the period of alcohol consumption increased, the positive rate of expression of hypoxia-inducible factor-1 alpha (HIF-1alpha) mRNA was more significantly elevated in the liver of the alcohol group than in the control group (P < or = 0.05).
  • [MeSH-major] Anoxia / metabolism. Ethanol / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Liver Diseases, Alcoholic / metabolism
  • [MeSH-minor] Animals. Male. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17085342.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 3K9958V90M / Ethanol
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36. Funchal C, Dos Santos AQ, Jacques-Silva MC, Zamoner A, Gottfried C, Wajner M, Pessoa-Pureur R: Branched-chain alpha-keto acids accumulating in maple syrup urine disease induce reorganization of phosphorylated GFAP in C6-glioma cells. Metab Brain Dis; 2005 Sep;20(3):205-17

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

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  • (PMID = 16167198.001).
  • [ISSN] 0885-7490
  • [Journal-full-title] Metabolic brain disease
  • [ISO-abbreviation] Metab Brain Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Keto Acids; 1460-34-0 / alpha-keto-beta-methylvaleric acid; 759-05-7 / alpha-ketoisovalerate; 816-66-0 / alpha-ketoisocaproic acid
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37. Hamm A, Veeck J, Bektas N, Wild PJ, Hartmann A, Heindrichs U, Kristiansen G, Werbowetski-Ogilvie T, Del Maestro R, Knuechel R, Dahl E: Frequent expression loss of Inter-alpha-trypsin inhibitor heavy chain (ITIH) genes in multiple human solid tumors: a systematic expression analysis. BMC Cancer; 2008;8:25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent expression loss of Inter-alpha-trypsin inhibitor heavy chain (ITIH) genes in multiple human solid tumors: a systematic expression analysis.
  • BACKGROUND: The inter-alpha-trypsin inhibitors (ITI) are a family of plasma protease inhibitors, assembled from a light chain - bikunin, encoded by AMBP - and five homologous heavy chains (encoded by ITIH1, ITIH2, ITIH3, ITIH4, and ITIH5), contributing to extracellular matrix stability by covalent linkage to hyaluronan.
  • METHODS: We systematically investigated differential gene expression of the ITIH gene family, as well as AMBP and the interacting partner TNFAIP6 in 13 different human tumor entities (of breast, endometrium, ovary, cervix, stomach, small intestine, colon, rectum, lung, thyroid, prostate, kidney, and pancreas) using cDNA dot blot analysis (Cancer Profiling Array, CPA), semiquantitative RT-PCR and immunohistochemistry.
  • [MeSH-major] Alpha-Globulins / metabolism. Breast Neoplasms / genetics. Carcinoma / genetics. Carcinoma / secondary. Carcinoma in Situ / genetics. Gene Expression Regulation, Neoplastic. Neoplasms / genetics

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  • [Cites] Biochem Biophys Res Commun. 2001 Nov 30;289(2):472-8 [11716497.001]
  • [Cites] J Rheumatol. 1987 Jun;14(3):439-45 [3625626.001]
  • [Cites] Crit Care Med. 2002 Mar;30(3):617-22 [11990925.001]
  • [Cites] Adv Enzyme Regul. 2002;42:63-82 [12123707.001]
  • [Cites] Reproduction. 2003 Jan;125(1):27-31 [12622693.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1571-5 [2894030.001]
  • [Cites] Cell. 1988 Feb 12;52(3):321-8 [3125981.001]
  • [Cites] Int J Biochem Cell Biol. 2000 Feb;32(2):125-37 [10687949.001]
  • [Cites] Am J Hum Genet. 2000 Nov;67(5):1047-54 [11001584.001]
  • [Cites] Biotechniques. 2001 Mar;30(3):512-6, 518-20 [11252787.001]
  • [Cites] Endocr Rev. 2001 Apr;22(2):184-204 [11294823.001]
  • [Cites] Eur J Biochem. 1989 Jan 15;179(1):147-54 [2465147.001]
  • [Cites] Eur J Biochem. 1989 May 15;181(3):571-6 [2471637.001]
  • [Cites] Ciba Found Symp. 1989;143:187-201; discussion 201-7, 281-5 [2478344.001]
  • [Cites] Genes Chromosomes Cancer. 1990 Jan;1(3):240-6 [1982064.001]
  • [Cites] Cancer Res. 1993 Dec 1;53(23):5775-9 [8242635.001]
  • [Cites] J Biol Chem. 1993 Dec 15;268(35):26725-30 [7504674.001]
  • [Cites] Biochem J. 1994 Sep 1;302 ( Pt 2):573-80 [7522438.001]
  • [Cites] J Biol Chem. 1995 Apr 7;270(14):8361-6 [7713945.001]
  • [Cites] Int J Cancer. 1995 Nov 3;63(3):455-62 [7591248.001]
  • [Cites] J Immunol. 1996 Feb 15;156(4):1609-15 [8568267.001]
  • [Cites] Biochem J. 1996 Apr 1;315 ( Pt 1):1-9 [8670091.001]
  • [Cites] Biol Pharm Bull. 1998 Feb;21(2):167-9 [9514613.001]
  • [Cites] Eur J Biochem. 1998 Mar 15;252(3):339-46 [9546647.001]
  • [Cites] Eur J Biochem. 1998 May 1;253(3):817-26 [9654084.001]
  • [Cites] J Steroid Biochem Mol Biol. 1998 Apr;65(1-6):163-8 [9699869.001]
  • [Cites] J Biol Chem. 1998 Oct 9;273(41):26809-19 [9756925.001]
  • [Cites] Nat Med. 1998 Nov;4(11):1329-33 [9809560.001]
  • [Cites] Urol Res. 1999;27(1):69-75 [10092156.001]
  • [Cites] Biol Reprod. 1999 Aug;61(2):436-43 [10411524.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Sep 16;263(1):224-9 [10486281.001]
  • [Cites] J Pathol. 2005 Jan;205(1):21-8 [15586368.001]
  • [Cites] J Biol Chem. 2005 Mar 25;280(12):11936-42 [15653696.001]
  • [Cites] J Biol Chem. 2005 Jul 8;280(27):25674-86 [15840581.001]
  • [Cites] Infect Immun. 2005 Aug;73(8):5101-5 [16041026.001]
  • [Cites] Int J Cancer. 2005 Dec 20;117(6):961-73 [15986450.001]
  • [Cites] Int J Cancer. 2006 Mar 15;118(6):1453-9 [16187283.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1464-72 [16452202.001]
  • [Cites] Mol Cell Endocrinol. 2006 Mar 9;247(1-2):53-9 [16426741.001]
  • [Cites] Clin Cancer Res. 2006 Jul 1;12(13):3950-60 [16818692.001]
  • [Cites] BMC Cancer. 2006;6:88 [16603086.001]
  • [Cites] Crit Care Med. 2007 Feb;35(2):387-92 [17205024.001]
  • [Cites] Mol Endocrinol. 2007 Sep;21(9):2112-23 [17550982.001]
  • [Cites] Oncogene. 2008 Jan 31;27(6):865-76 [17653090.001]
  • [Cites] J Cell Sci. 2003 May 15;116(Pt 10):1863-73 [12692188.001]
  • [Cites] Cell Mol Life Sci. 2003 Mar;60(3):463-73 [12737307.001]
  • [Cites] Biol Chem. 2003 May;384(5):749-54 [12817471.001]
  • [Cites] Am J Pathol. 2003 Jul;163(1):121-33 [12819017.001]
  • [Cites] J Infect Dis. 2003 Sep 15;188(6):919-26 [12964125.001]
  • [Cites] Glycoconj J. 2002 May-Jun;19(4-5):241-7 [12975601.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6105-9 [14559785.001]
  • [Cites] Osteoarthritis Cartilage. 2004 Feb;12(2):142-8 [14723873.001]
  • [Cites] Cancer Lett. 2004 Feb 10;204(1):69-77 [14744536.001]
  • [Cites] J Biol Chem. 2004 Feb 20;279(8):6371-9 [14597629.001]
  • [Cites] J Biol Chem. 2004 Mar 19;279(12):11119-28 [14707130.001]
  • [Cites] J Biol Chem. 2004 Sep 10;279(37):38079-82 [15151994.001]
  • [Cites] Methods Enzymol. 1976;45:760-72 [64916.001]
  • [Cites] Dig Dis Sci. 1984 Jan;29(1):26-32 [6363018.001]
  • [Cites] Cell. 1986 Sep 26;46(7):1053-61 [3463433.001]
  • [Cites] Pathologe. 1987 May;8(3):138-40 [3303008.001]
  • [Cites] Int J Cancer. 2002 Feb 10;97(5):615-20 [11807786.001]
  • (PMID = 18226209.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alpha-Globulins; 0 / RNA, Messenger; 39346-44-6 / inter-alpha-inhibitor
  • [Other-IDs] NLM/ PMC2268946
  •  go-up   go-down


38. Kiebala M, Polesskaya O, Yao Z, Perry SW, Maggirwar SB: Nuclear factor-kappa B family member RelB inhibits human immunodeficiency virus-1 Tat-induced tumor necrosis factor-alpha production. PLoS One; 2010 Jul 29;5(7):e11875
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nuclear factor-kappa B family member RelB inhibits human immunodeficiency virus-1 Tat-induced tumor necrosis factor-alpha production.
  • Human Immunodeficiency Virus-1 (HIV-1)-associated neurocognitive disorder (HAND) is likely neuroinflammatory in origin, believed to be triggered by inflammatory and oxidative stress responses to cytokines and HIV protein gene products such as the HIV transactivator of transcription (Tat).
  • Indeed, tumor necrosis factor-alpha (TNFalpha) production in monocytes isolated from RelB deficient mice was significantly higher than in monocytes isolated from RelB expressing controls.

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  • [Cites] Am J Pathol. 2002 Feb;160(2):559-67 [11839576.001]
  • [Cites] Am J Pathol. 2002 Mar;160(3):927-41 [11891191.001]
  • [Cites] AIDS. 2002 May 3;16(7):1019-29 [11953468.001]
  • [Cites] Cell. 2002 Apr;109 Suppl:S81-96 [11983155.001]
  • [Cites] J Neurol Sci. 2002 Oct 15;202(1-2):13-23 [12220687.001]
  • [Cites] J Neurovirol. 2002 Dec;8(6):611-24 [12476354.001]
  • [Cites] Clin Diagn Lab Immunol. 2003 Jan;10(1):133-9 [12522051.001]
  • [Cites] J Exp Med. 1992 Dec 1;176(6):1703-18 [1460427.001]
  • [Cites] Mol Cell Biol. 1993 Mar;13(3):1572-82 [8441398.001]
  • [Cites] Am J Pathol. 1997 Aug;151(2):375-87 [9250151.001]
  • [Cites] J Biol Chem. 1997 Sep 5;272(36):22385-8 [9278385.001]
  • [Cites] AIDS. 1997 Oct;11(12):1421-31 [9342064.001]
  • [Cites] Ann Neurol. 1997 Dec;42(6):963-72 [9403489.001]
  • [Cites] Prog Neurobiol. 1998 Jan;54(1):19-33 [9460791.001]
  • [Cites] Annu Rev Immunol. 1998;16:225-60 [9597130.001]
  • [Cites] Clin Infect Dis. 1998 May;26(5):1072-3 [9597227.001]
  • [Cites] J Biol Chem. 1998 Jul 10;273(28):17660-4 [9651362.001]
  • [Cites] J Biol Chem. 1999 Jun 11;274(24):17098-102 [10358063.001]
  • [Cites] Brain Res Dev Brain Res. 1999 Jun 8;115(1):71-81 [10366704.001]
  • [Cites] J Biol Chem. 1999 Oct 8;274(41):28837-40 [10506122.001]
  • [Cites] Mol Cell Biol. 1999 Nov;19(11):7688-96 [10523657.001]
  • [Cites] Virology. 2004 Nov 24;329(2):371-80 [15518816.001]
  • [Cites] J Immunol. 2004 Dec 1;173(11):6735-44 [15557166.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):51545-53 [15452123.001]
  • [Cites] J Neuroimmunol. 2004 Dec;157(1-2):3-10 [15579274.001]
  • [Cites] Nat Rev Immunol. 2005 Jan;5(1):69-81 [15630430.001]
  • [Cites] Glia. 2005 Mar;49(4):501-10 [15578658.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14635-40 [16192349.001]
  • [Cites] Curr Pharm Des. 2006;12(9):1023-44 [16515484.001]
  • [Cites] J Immunol. 2006 Jul 1;177(1):702-11 [16785569.001]
  • [Cites] Mol Cell. 2003 Jun;11(6):1563-74 [12820969.001]
  • [Cites] J Immunol. 2003 Sep 15;171(6):3136-41 [12960340.001]
  • [Cites] J Virol. 2004 Mar;78(5):2586-90 [14963162.001]
  • [Cites] Arch Neurol. 2004 Mar;61(3):369-76 [15023814.001]
  • [Cites] J Neurovirol. 2004 Apr;10(2):86-97 [15204927.001]
  • [Cites] J Neurovirol. 2004 Aug;10(4):223-32 [15371152.001]
  • [Cites] EMBO J. 2004 Oct 27;23(21):4202-10 [15470505.001]
  • [Cites] Neurology. 1988 Jan;38(1):9-14 [3422110.001]
  • [Cites] Science. 1988 Apr 1;240(4848):70-3 [2832944.001]
  • [Cites] J Virol. 1989 Jan;63(1):1-8 [2535718.001]
  • [Cites] J Cell Biol. 1990 Sep;111(3):1275-81 [2202737.001]
  • [Cites] FASEB J. 1991 Jul;5(10):2391-7 [2065887.001]
  • [Cites] Ann Neurol. 1991 Jun;29(6):651-7 [1909852.001]
  • [Cites] J Biol Chem. 1998 Jul 10;273(28):17852-8 [9651389.001]
  • [Cites] Neuroimmunomodulation. 1998 May-Aug;5(3-4):184-92 [9730685.001]
  • [Cites] J Neurosci. 1998 Dec 15;18(24):10356-65 [9852573.001]
  • [Cites] Brain Pathol. 1999 Apr;9(2):209-17 [10219738.001]
  • [Cites] Eur J Clin Invest. 2006 Jul;36(7):447-58 [16796601.001]
  • [Cites] Curr HIV Res. 2006 Jul;4(3):307-18 [16842083.001]
  • [Cites] Retrovirology. 2006;3:28 [16712719.001]
  • [Cites] J Cereb Blood Flow Metab. 2006 Aug;26(8):1052-65 [16395283.001]
  • [Cites] Curr Opin Neurol. 2006 Aug;19(4):358-61 [16914973.001]
  • [Cites] J Immunol. 2006 Sep 15;177(6):4080-5 [16951372.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Mar 15;90(6):2335-9 [7681592.001]
  • [Cites] Biochem Biophys Res Commun. 1994 Aug 30;203(1):623-30 [8074713.001]
  • [Cites] EMBO J. 1994 Sep 1;13(17):4060-9 [8076601.001]
  • [Cites] Cell. 1995 Jan 27;80(2):331-40 [7834753.001]
  • [Cites] Dev Neurosci. 1993;15(6):417-22 [7835247.001]
  • [Cites] EMBO J. 1995 Feb 1;14(3):546-54 [7859743.001]
  • [Cites] Acta Neuropathol. 1994;88(6):538-44 [7879600.001]
  • [Cites] Nature. 1995 Jun 8;375(6531):497-500 [7539892.001]
  • [Cites] Immunobiology. 1995 Jul;193(2-4):193-203 [8530143.001]
  • [Cites] Ann Neurol. 1995 Nov;38(5):755-62 [7486867.001]
  • [Cites] Virology. 1996 Feb 1;216(1):284-7 [8615004.001]
  • [Cites] J Biol Chem. 1996 Jun 28;271(26):15303-6 [8663435.001]
  • [Cites] J Virol. 1996 Sep;70(9):5777-85 [8709193.001]
  • [Cites] Eur Cytokine Netw. 1997 Mar;8(1):37-43 [9110146.001]
  • [Cites] J Immunol. 1997 Jun 1;158(11):5211-8 [9164938.001]
  • [Cites] J Immunol. 2007 Mar 1;178(5):3226-36 [17312171.001]
  • [Cites] J Acquir Immune Defic Syndr. 2007 Jun 1;45(2):174-82 [17356465.001]
  • [Cites] Curr Protoc Cell Biol. 2001 May;Chapter 2:Unit 2.2 [18228347.001]
  • [Cites] Int Rev Psychiatry. 2008 Feb;20(1):15-24 [18240059.001]
  • [Cites] Behav Brain Res. 2008 Apr 9;188(2):337-47 [18242723.001]
  • [Cites] Cell. 2008 Feb 8;132(3):344-62 [18267068.001]
  • [Cites] Curr HIV Res. 2008 Mar;6(2):117-29 [18336259.001]
  • [Cites] J Neuroinflammation. 2008;5:13 [18400101.001]
  • [Cites] Cell Mol Life Sci. 2008 Oct;65(19):2964-78 [18535784.001]
  • [Cites] J Neurosci. 2008 Nov 19;28(47):12190-8 [19020013.001]
  • [Cites] Nat Immunol. 2009 Feb;10(2):203-13 [19122653.001]
  • [Cites] EMBO Rep. 2009 Feb;10(2):152-9 [19098713.001]
  • [Cites] Exp Mol Med. 2009 Feb 28;41(2):86-93 [19287189.001]
  • [Cites] Annu Rev Immunol. 2009;27:693-733 [19302050.001]
  • [Cites] Top HIV Med. 2009 Apr-May;17(2):46-56 [19401607.001]
  • [Cites] Curr Opin Neurol. 2009 Jun;22(3):315-20 [19300249.001]
  • [Cites] J Neurovirol. 2009 Apr;15(2):187-95 [19306228.001]
  • [Cites] Clin Neurol Neurosurg. 2009 Jun;111(5):422-9 [19185416.001]
  • [Cites] Neuroimage. 2009 Oct 1;47(4):1154-62 [19376246.001]
  • [Cites] Annu Rev Med. 2010;61:35-47 [19719397.001]
  • [Cites] Am J Pathol. 2010 Feb;176(2):893-902 [20035054.001]
  • [Cites] Neuropsychologia. 2010 Mar;48(4):1133-43 [20018201.001]
  • [Cites] J Neurovirol. 2009 Jul;15(4):324-33 [19499454.001]
  • [Cites] AIDS. 2009 Sep 24;23(15):1977-85 [19730350.001]
  • [Cites] Biomed Pharmacother. 2003 Jan;57(1):49-56 [12642037.001]
  • [Cites] Am J Pathol. 2003 May;162(5):1693-707 [12707054.001]
  • [Cites] J Neurovirol. 2003 Apr;9(2):205-21 [12707851.001]
  • [Cites] Brain Pathol. 2003 Apr;13(2):195-210 [12744473.001]
  • [Cites] J Biol Chem. 2003 May 30;278(22):19852-60 [12657634.001]
  • [Cites] Mol Cell Biol. 2003 Jul;23(13):4649-62 [12808104.001]
  • [Cites] J Virol. 1991 Nov;65(11):6094-100 [1920627.001]
  • [Cites] J Neurochem. 2000 Feb;74(2):527-39 [10646503.001]
  • [Cites] Ann Neurol. 2000 Feb;47(2):186-94 [10665489.001]
  • [Cites] AIDS. 2000 Jan 7;14(1):69-74 [10714569.001]
  • [Cites] Annu Rev Immunol. 2000;18:621-63 [10837071.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11466-71 [11027346.001]
  • [Cites] Nature. 2001 Apr 19;410(6831):988-94 [11309629.001]
  • [Cites] Oncogene. 2001 Nov 22;20(53):7722-33 [11753650.001]
  • [Cites] J Biol Chem. 2002 Jan 11;277(2):1405-18 [11687592.001]
  • (PMID = 20686703.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / R21 DA030256; United States / NIMH NIH HHS / MH / R21 MH084718-02; United States / NINDS NIH HHS / NS / R01 NS054578; United States / NIAID NIH HHS / AI / T32 AI049815; United States / NIMH NIH HHS / MH / R21 MH084718; United States / NINDS NIH HHS / NS / R01 NS066801; United States / NIAID NIH HHS / AI / T32 AI49105; United States / NIDA NIH HHS / DA / R21 DA030256-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha; 0 / tat Gene Products, Human Immunodeficiency Virus; 147337-75-5 / Transcription Factor RelB
  • [Other-IDs] NLM/ PMC2912378
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39. Bennett CE, Nsengimana J, Bostock JA, Cymbalista C, Futers TS, Knight BL, McCormack LJ, Prasad UK, Riches K, Rolton D, Scarrott T, Barrett JH, Carter AM: CCAAT/enhancer binding protein alpha, beta and delta gene variants: associations with obesity related phenotypes in the Leeds Family Study. Diab Vasc Dis Res; 2010 Jul;7(3):195-203
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  • [Title] CCAAT/enhancer binding protein alpha, beta and delta gene variants: associations with obesity related phenotypes in the Leeds Family Study.
  • OBJECTIVE: To identify novel polymorphisms in the genes encoding the transcription factors CCAAT/enhancer binding protein alpha, beta and delta ( CEBPA, CEBPB, CEBPD) and investigate associations between polymorphisms and obesity-related phenotypes.
  • CONCLUSION: These findings suggest that common allelic variants in CEBPA and CEBPB could influence abdominal obesity and related metabolic abnormalities associated with type 2 diabetes and cardiovascular disease in healthy White Northern European families, although results require independent confirmation.
  • [MeSH-minor] Adiponectin / blood. Chromatography, High Pressure Liquid. England / epidemiology. European Continental Ancestry Group / genetics. Genetic Predisposition to Disease. Haplotypes. Humans. Leptin / blood. Linear Models. Linkage Disequilibrium. Pedigree. Phenotype. Polymerase Chain Reaction. Risk Assessment. Risk Factors. Waist-Hip Ratio

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  • (PMID = 20460359.001).
  • [ISSN] 1752-8984
  • [Journal-full-title] Diabetes & vascular disease research
  • [ISO-abbreviation] Diab Vasc Dis Res
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 067867; United Kingdom / British Heart Foundation / / FS2001/037
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ADIPOQ protein, human; 0 / Adiponectin; 0 / CCAAT-Enhancer-Binding Protein-beta; 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / CEBPB protein, human; 0 / CEBPD protein, human; 0 / Leptin; 142662-43-9 / CCAAT-Enhancer-Binding Protein-delta
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40. Dai CX, Gao Q, Qiu SJ, Ju MJ, Cai MY, Xu YF, Zhou J, Zhang BH, Fan J: Hypoxia-inducible factor-1 alpha, in association with inflammation, angiogenesis and MYC, is a critical prognostic factor in patients with HCC after surgery. BMC Cancer; 2009;9:418
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  • [Title] Hypoxia-inducible factor-1 alpha, in association with inflammation, angiogenesis and MYC, is a critical prognostic factor in patients with HCC after surgery.
  • BACKGROUND: Despite well-studied tumor hypoxia in laboratory, little is known about the association with other pathophysiological events in the clinical view.
  • We investigated the prognostic value of hypoxia-inducible factor-1 alpha (HIF-1alpha) in hepatocellular carcinoma (HCC), and its correlations with inflammation, angiogenesis and MYC oncogene.
  • RESULTS: The expression of both HIF-1alpha mRNA and protein in HCC were independent prognostic factors for overall survival (OS) (P = 0.012 and P = 0.021, respectively) and disease-free survival (DFS) (P = 0.004 and P = 0.007, respectively) as well.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Inflammation / metabolism. Liver Neoplasms / metabolism. Neovascularization, Pathologic / pathology. Proto-Oncogene Proteins c-myc / biosynthesis
  • [MeSH-minor] Biomarkers, Tumor / analysis. Disease-Free Survival. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Tissue Array Analysis

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  • [Cites] Cancer Res. 1999 Nov 15;59(22):5830-5 [10582706.001]
  • [Cites] Front Biosci (Landmark Ed). 2009;14:3094-110 [19273260.001]
  • [Cites] Arch Orthop Trauma Surg. 2001;121(4):219-22 [11317684.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1158-65 [11861398.001]
  • [Cites] J Mol Med (Berl). 2002 Nov;80(11):703-14 [12436347.001]
  • [Cites] FASEB J. 2003 Sep;17(12):1709-11 [12958184.001]
  • [Cites] Cancer Treat Res. 2004;117:219-48 [15015563.001]
  • [Cites] Circ Res. 2004 May 14;94(9):1186-94 [15059936.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5496-503 [15289360.001]
  • [Cites] J Biol Chem. 1997 Jan 3;272(1):601-8 [8995303.001]
  • [Cites] Semin Liver Dis. 1999;19(3):329-38 [10518312.001]
  • [Cites] Clin Cancer Res. 2004 Nov 1;10(21):7252-9 [15534099.001]
  • [Cites] J Hepatol. 2005 Mar;42(3):358-64 [15710218.001]
  • [Cites] Digestion. 2005;71(2):124-30 [15785038.001]
  • [Cites] Kidney Int. 2005 Aug;68(2):695-703 [16014047.001]
  • [Cites] Physiol Genomics. 2005 Aug 11;22(3):308-18 [15942021.001]
  • [Cites] Exp Oncol. 2005 Sep;27(3):202-5 [16244581.001]
  • [Cites] Cancer Treat Rev. 2006 Feb;32(1):28-44 [16337744.001]
  • [Cites] Mol Interv. 2006 Aug;6(4):199-207 [16960142.001]
  • [Cites] Int J Oncol. 2006 Dec;29(6):1533-9 [17088993.001]
  • [Cites] Res Commun Mol Pathol Pharmacol. 2004;115-116:143-50 [17564313.001]
  • [Cites] J Clin Oncol. 2007 Jun 20;25(18):2586-93 [17577038.001]
  • [Cites] J Gastroenterol Hepatol. 2007 Aug;22(8):1178-82 [17559361.001]
  • [Cites] Cancer Cell. 2007 Aug;12(2):108-13 [17692803.001]
  • [Cites] Bull Cancer. 2007 Jul;94 Spec No:S160-5 [17846000.001]
  • [Cites] Clin Cancer Res. 2007 Dec 15;13(24):7388-93 [18094421.001]
  • [Cites] Nat Rev Cancer. 2008 Jan;8(1):51-6 [18046334.001]
  • [Cites] Nature. 2008 Feb 21;451(7181):1008-12 [18288196.001]
  • [Cites] Rev Recent Clin Trials. 2008 Jan;3(1):31-9 [18474013.001]
  • [Cites] Neoplasia. 2008 Jul;10(7):674-9 [18592007.001]
  • [Cites] J Cancer Res Clin Oncol. 2008 Sep;134(9):979-86 [18317805.001]
  • [Cites] J Physiol. 2008 Sep 1;586(Pt 17):4055-9 [18599532.001]
  • [Cites] Dig Dis Sci. 2008 Dec;53(12):3225-33 [18465238.001]
  • [Cites] Cancer Sci. 2008 Oct;99(10):2055-61 [19016766.001]
  • [Cites] Nat Rev Cancer. 2008 Dec;8(12):967-75 [18987634.001]
  • [Cites] Gastroenterology. 2009 Feb;136(2):585-95.e5 [19013462.001]
  • [Cites] Clin Cancer Res. 2009 Feb 1;15(3):971-9 [19188168.001]
  • [Cites] J Hepatol. 2001 Feb;34(2):239-47 [11281552.001]
  • (PMID = 19948069.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Proto-Oncogene Proteins c-myc
  • [Other-IDs] NLM/ PMC2797816
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41. Ripoli M, D'Aprile A, Quarato G, Sarasin-Filipowicz M, Gouttenoire J, Scrima R, Cela O, Boffoli D, Heim MH, Moradpour D, Capitanio N, Piccoli C: Hepatitis C virus-linked mitochondrial dysfunction promotes hypoxia-inducible factor 1 alpha-mediated glycolytic adaptation. J Virol; 2010 Jan;84(1):647-60
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  • [Title] Hepatitis C virus-linked mitochondrial dysfunction promotes hypoxia-inducible factor 1 alpha-mediated glycolytic adaptation.
  • Hepatitis C virus (HCV) infection induces a state of oxidative stress by affecting mitochondrial-respiratory-chain activity.
  • Here, we show that HCV protein expression activates hypoxia-inducible factor 1 (HIF-1) by normoxic stabilization of its alpha subunit.
  • [MeSH-major] Adaptation, Physiological. Glycolysis. Hepacivirus / pathogenicity. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Mitochondria / virology

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  • [Cites] Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1765-74 [16987030.001]
  • [Cites] Hepatology. 1998 Jul;28(1):192-201 [9657112.001]
  • [Cites] EMBO J. 2000 Aug 15;19(16):4298-309 [10944113.001]
  • [Cites] Science. 1997 Jul 25;277(5325):570-4 [9228008.001]
  • [Cites] Biochim Biophys Acta. 2009 May;1787(5):539-46 [19094961.001]
  • [Cites] J Hepatol. 2004 Nov;41(5):864-80 [15519663.001]
  • [Cites] Science. 1956 Aug 10;124(3215):269-70 [13351639.001]
  • [Cites] Int J Biochem Cell Biol. 2005 Mar;37(3):535-40 [15618010.001]
  • [Cites] Front Biosci. 2005;10:1881-96 [15769673.001]
  • [Cites] Trends Microbiol. 2005 Apr;13(4):159-63 [15817385.001]
  • [Cites] J Med Virol. 2005 Aug;76(4):489-97 [15977232.001]
  • [Cites] Science. 2005 Jul 22;309(5734):623-6 [15947137.001]
  • [Cites] J Cell Biochem. 2005 Aug 15;95(6):1264-75 [15962286.001]
  • [Cites] Lancet Infect Dis. 2005 Sep;5(9):558-67 [16122679.001]
  • [Cites] Exp Physiol. 2005 Nov;90(6):791-7 [16157658.001]
  • [Cites] J Biol Chem. 2005 Dec 23;280(51):41928-39 [16223732.001]
  • [Cites] J Biol Chem. 2006 Apr 14;281(15):9833-6 [16407182.001]
  • [Cites] Oncogene. 2006 Jun 26;25(27):3834-47 [16799625.001]
  • [Cites] Oncogene. 2006 Aug 7;25(34):4675-82 [16892081.001]
  • [Cites] J Biol Chem. 2001 Nov 23;276(47):44052-63 [11557752.001]
  • [Cites] J Biol Chem. 2002 Mar 8;277(10):8130-9 [11744739.001]
  • [Cites] J Biol Chem. 2002 Oct 11;277(41):38205-11 [12149254.001]
  • [Cites] J Virol. 2002 Dec;76(24):13001-14 [12438626.001]
  • [Cites] Curr Med Chem. 2003 Jun;10(12):1005-19 [12678673.001]
  • [Cites] Nat Rev Cancer. 2003 Oct;3(10):721-32 [13130303.001]
  • [Cites] J Biol Chem. 2003 Oct 3;278(40):39076-84 [12855680.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):985-93 [14871829.001]
  • [Cites] Nat Rev Mol Cell Biol. 2004 May;5(5):343-54 [15122348.001]
  • [Cites] J Virol. 2004 Aug;78(15):7958-68 [15254168.001]
  • [Cites] Curr Med Chem. 2004 Aug;11(16):2195-204 [15279558.001]
  • [Cites] J Biol Chem. 1994 Sep 23;269(38):23757-63 [8089148.001]
  • [Cites] J Biol Chem. 1995 Sep 8;270(36):21021-7 [7673128.001]
  • [Cites] Virology. 1996 Aug 1;222(1):51-63 [8806487.001]
  • [Cites] Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1791-806 [16987032.001]
  • [Cites] Biochim Biophys Acta. 2006 Sep-Oct;1757(9-10):1429-37 [16814246.001]
  • [Cites] Cancer Res. 2006 Dec 1;66(23):11263-70 [17145871.001]
  • [Cites] FEBS J. 2007 Jan;274(1):1-22 [17222174.001]
  • [Cites] J Biol Chem. 2007 Feb 16;282(7):4524-32 [17182618.001]
  • [Cites] J Virol. 2007 May;81(9):4591-603 [17301154.001]
  • [Cites] Nat Rev Microbiol. 2007 Jun;5(6):453-63 [17487147.001]
  • [Cites] Hepatology. 2007 Jul;46(1):58-65 [17567832.001]
  • [Cites] FASEB J. 2007 Aug;21(10):2474-85 [17392480.001]
  • [Cites] J Virol. 2007 Oct;81(19):10249-57 [17626077.001]
  • [Cites] Methods Enzymol. 2007;435:463-78 [17998069.001]
  • [Cites] Cell Death Differ. 2008 Apr;15(4):678-85 [18259193.001]
  • [Cites] Cell Death Differ. 2008 Apr;15(4):635-41 [18259202.001]
  • [Cites] Anticancer Agents Med Chem. 2008 Apr;8(3):305-12 [18393789.001]
  • [Cites] Biochem J. 2008 Jun 15;412(3):477-84 [18393939.001]
  • [Cites] Carcinogenesis. 2008 Aug;29(8):1528-37 [18515279.001]
  • [Cites] J Biol Chem. 2009 Feb 13;284(7):4123-31 [19097995.001]
  • [Cites] J Virol. 2009 May;83(10):5137-47 [19264780.001]
  • [Cites] J Virol. 2000 Mar;74(5):2293-304 [10666260.001]
  • (PMID = 19846525.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC2798449
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42. Osei K, Gaillard T, Cook C, Kaplow J, Bullock M, Schuster D: Discrepancies in the regulation of plasma adiponectin and TNF-alpha levels and adipose tissue gene expression in obese African Americans with glucose intolerance: a pilot study using rosiglitazone. Ethn Dis; 2005;15(4):641-8
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  • [Title] Discrepancies in the regulation of plasma adiponectin and TNF-alpha levels and adipose tissue gene expression in obese African Americans with glucose intolerance: a pilot study using rosiglitazone.
  • 1) on glucose homeostasis, insulin action, beta-cell function, and plasma adiponectin and TNF-alpha (TNF-alpha) levels; and 2) the expression of adipose tissue TNF-alpha and adiponectin mRNA in African Americans with parental history of type 2 diabetes and with varying degrees of glucose intolerance.
  • Adipose tissue gene expression (mRNA) was measured by real-time polymerase chain reaction in both groups.
  • Mean plasma TNF-alpha levels were not significantly different at fasting and after two hours during OGTT.
  • Rosiglitazone had no significant effect on plasma TNF-alpha levels during OGTT.
  • No significant differences were seen in the expression of adipose tissue TNF-alpha and adiponectin mRNA in the groups at baseline.
  • Rosiglitazone did not significantly change the adipose tissue adiponectin and TNF-alpha mRNA.
  • Rosiglitazone was well tolerated, without experiencing weight gain, edema, and liver function test abnormality in the glucose intolerant subjects.
  • We found that adiponectin was lower in the glucose-intolerant group, while TNF-alpha was similar.
  • In addition, rosiglitazone had no effect on plasma TNF-alpha and adipose tissue TNF-alpha mRNA.
  • We conclude that the metabolic effects of rosiglitazone could be mediated by adiponectin but not TNF-alpha in African Americans with glucose intolerance.
  • 1) the role of adipocytokines in the etiology of type 2 diabetes in African Americans is complex; and 2) that adiponectin, but not TNF-alpha, could mediate the metabolic benefits of thiazolidinediones in African Americans with glucose intolerance.
  • [MeSH-major] Adiponectin / blood. Adipose Tissue / metabolism. African Americans. Obesity / genetics. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Adult. Blood Glucose / metabolism. Cholesterol, HDL / blood. Cholesterol, LDL / blood. Diabetes Mellitus, Type 2 / drug therapy. Diabetes Mellitus, Type 2 / ethnology. Diabetes Mellitus, Type 2 / genetics. Female. Gene Expression / drug effects. Glucose Intolerance / ethnology. Glucose Intolerance / genetics. Glucose Tolerance Test. Humans. Hypoglycemic Agents / administration & dosage. Hypoglycemic Agents / therapeutic use. Longitudinal Studies. Male. Middle Aged. Pilot Projects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Thiazolidinediones / administration & dosage. Thiazolidinediones / therapeutic use

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  • [CommentIn] Ethn Dis. 2005 Autumn;15(4):802-3 [16261688.001]
  • (PMID = 16259488.001).
  • [ISSN] 1049-510X
  • [Journal-full-title] Ethnicity & disease
  • [ISO-abbreviation] Ethn Dis
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK48127; United States / CCR NIH HHS / RC / GCRC-RR0034; United States / PHS HHS / / KO8
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Blood Glucose; 0 / Cholesterol, HDL; 0 / Cholesterol, LDL; 0 / Hypoglycemic Agents; 0 / RNA, Messenger; 0 / Thiazolidinediones; 0 / Tumor Necrosis Factor-alpha; 05V02F2KDG / rosiglitazone
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43. Hui W, Barksby HE, Young DA, Cawston TE, McKie N, Rowan AD: Oncostatin M in combination with tumour necrosis factor {alpha} induces a chondrocyte membrane associated aggrecanase that is distinct from ADAMTS aggrecanase-1 or -2. Ann Rheum Dis; 2005 Nov;64(11):1624-32
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  • [Title] Oncostatin M in combination with tumour necrosis factor {alpha} induces a chondrocyte membrane associated aggrecanase that is distinct from ADAMTS aggrecanase-1 or -2.
  • OBJECTIVE: To determine whether oncostatin M (OSM) + tumour necrosis factor alpha (TNFalpha) induces aggrecanase activity in chondrocyte membranes, to determine the effects of transforming growth factor beta1 (TGFbeta1), interleukin 4 (IL4), and tissue inhibitor of metalloproteinases (TIMPs) on this activity, and to determine whether this activity is due to a known ADAMTS aggrecanase.
  • Expression of known aggrecanases was measured by real time polymerase chain reaction in bovine nasal and human articular chondrocytes.

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  • [Cites] Arthritis Rheum. 2002 Apr;46(4):961-7 [11953973.001]
  • [Cites] J Biol Chem. 2002 Mar 29;277(13):11034-41 [11796708.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Apr 26;293(1):501-8 [12054629.001]
  • [Cites] J Biol Chem. 2002 Jun 21;277(25):22201-8 [11956193.001]
  • [Cites] Ann Rheum Dis. 2002 Aug;61(8):704-13 [12117676.001]
  • [Cites] Arthritis Rheum. 2002 Oct;46(10):2648-57 [12384923.001]
  • [Cites] Cytokine Growth Factor Rev. 2002 Jun;13(3):241-57 [12486877.001]
  • [Cites] Ann Rheum Dis. 2003 Feb;62(2):172-4 [12525389.001]
  • [Cites] Arthritis Rheum. 2003 Jan;48(1):119-33 [12528112.001]
  • [Cites] J Biol Chem. 2003 Mar 14;278(11):9503-13 [12514189.001]
  • [Cites] Arthritis Rheum. 2003 Apr;48(4):1057-66 [12687549.001]
  • [Cites] Arthritis Res Ther. 2003;5(2):94-103 [12718749.001]
  • [Cites] Am J Pathol. 2003 Jun;162(6):1975-84 [12759253.001]
  • [Cites] Biochim Biophys Acta. 2003 May 20;1638(1):20-8 [12757930.001]
  • [Cites] Biochem Soc Symp. 2003;(70):115-23 [14587287.001]
  • [Cites] Arthritis Rheum. 2003 Dec;48(12):3404-18 [14673992.001]
  • [Cites] FEBS Lett. 2003 Dec 18;555(3):431-6 [14675751.001]
  • [Cites] Arthritis Rheum. 2004 Jan;50(1):131-41 [14730609.001]
  • [Cites] J Biol Chem. 2004 Mar 12;279(11):10042-51 [14701864.001]
  • [Cites] Osteoarthritis Cartilage. 2004 Apr;12(4):296-305 [15023381.001]
  • [Cites] Matrix Biol. 2004 Jul;23(4):219-30 [15296936.001]
  • [Cites] J Biol Chem. 1969 May 10;244(9):2384-96 [5783840.001]
  • [Cites] Biochem J. 1980 Aug 15;190(2):431-8 [7470058.001]
  • [Cites] Biochem J. 1983 Oct 15;216(1):27-36 [6316938.001]
  • [Cites] Nature. 1986 Aug 7-13;322(6079):547-9 [3736671.001]
  • [Cites] J Biol Chem. 1988 Mar 15;263(8):3632-8 [3346212.001]
  • [Cites] Biochem J. 1992 Jul 1;285 ( Pt 1):143-7 [1637293.001]
  • [Cites] J Clin Invest. 1997 Jul 1;100(1):93-106 [9202061.001]
  • [Cites] Br J Rheumatol. 1997 Jun;36(6):643-50 [9236673.001]
  • [Cites] Mol Pathol. 1997 Jun;50(3):153-9 [9292151.001]
  • [Cites] Arthritis Rheum. 1998 Oct;41(10):1760-71 [9778217.001]
  • [Cites] Biochem J. 1998 Nov 15;336 ( Pt 1):207-12 [9806902.001]
  • [Cites] Eur J Biochem. 1998 Nov 1;257(3):562-9 [9839944.001]
  • [Cites] J Biol Chem. 1999 Mar 5;274(10):6594-601 [10037754.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Feb 24;255(3):686-91 [10049771.001]
  • [Cites] Science. 1999 Jun 4;284(5420):1664-6 [10356395.001]
  • [Cites] Rheumatol Int. 1999;18(5-6):183-91 [10399794.001]
  • [Cites] Ann N Y Acad Sci. 1999 Jun 30;878:120-9 [10415724.001]
  • [Cites] J Biol Chem. 1999 Aug 13;274(33):23349-57 [10438512.001]
  • [Cites] J Biol Chem. 1999 Aug 13;274(33):23443-50 [10438522.001]
  • [Cites] Biochem J. 2005 Feb 15;386(Pt 1):15-27 [15554875.001]
  • [Cites] Arthritis Rheum. 2000 Feb;43(2):281-8 [10693867.001]
  • [Cites] Cytokine. 2000 Jun;12(6):765-9 [10843761.001]
  • [Cites] Genomics. 2000 Aug 1;67(3):343-50 [10936055.001]
  • [Cites] J Biol Chem. 2000 Aug 18;275(33):25791-7 [10827174.001]
  • [Cites] Arthritis Rheum. 2000 Sep;43(9):2100-9 [11014362.001]
  • [Cites] Matrix Biol. 2000 Nov;19(6):549-53 [11068209.001]
  • [Cites] Ann Rheum Dis. 2001 Feb;60(2):150-7 [11156549.001]
  • [Cites] Eur J Biochem. 2001 Mar;268(5):1259-68 [11231277.001]
  • [Cites] J Biol Chem. 2001 Apr 20;276(16):12501-4 [11278243.001]
  • [Cites] FEBS Lett. 2001 Apr 13;494(3):192-5 [11311239.001]
  • [Cites] Biochim Biophys Acta. 2001 May 3;1526(2):147-58 [11325536.001]
  • [Cites] Biochem J. 2001 Sep 15;358(Pt 3):615-26 [11535123.001]
  • [Cites] Cytokine. 2001 Oct 7;16(1):31-5 [11669584.001]
  • [Cites] Arthritis Rheum. 2001 Nov;44(11):2697-702 [11710726.001]
  • [Cites] J Immunol. 2002 Feb 1;168(3):1405-12 [11801682.001]
  • [Cites] Biochem J. 2002 Mar 1;362(Pt 2):465-72 [11853556.001]
  • [Cites] Biochem J. 2002 Mar 1;362(Pt 2):473-9 [11853557.001]
  • [Cites] Osteoarthritis Cartilage. 2002 Mar;10(3):234-43 [11869085.001]
  • [Cites] Matrix Biol. 2002 Apr;21(3):271-88 [12009333.001]
  • (PMID = 15883123.001).
  • [ISSN] 0003-4967
  • [Journal-full-title] Annals of the rheumatic diseases
  • [ISO-abbreviation] Ann. Rheum. Dis.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / OSM protein, human; 0 / Peptides; 0 / RNA, Messenger; 0 / Tissue Inhibitor of Metalloproteinase-3; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 106956-32-5 / Oncostatin M; 207137-56-2 / Interleukin-4; EC 3.4.- / Endopeptidases; EC 3.4.99.- / aggrecanase
  • [Other-IDs] NLM/ PMC1755260
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44. Voigt H, Lemke AK, Mentlein R, Schünke M, Kurz B: Tumor necrosis factor alpha-dependent aggrecan cleavage and release of glycosaminoglycans in the meniscus is mediated by nitrous oxide-independent aggrecanase activity in vitro. Arthritis Res Ther; 2009;11(5):R141
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  • [Title] Tumor necrosis factor alpha-dependent aggrecan cleavage and release of glycosaminoglycans in the meniscus is mediated by nitrous oxide-independent aggrecanase activity in vitro.
  • TNFalpha increased matrix metalloproteinase (MMP)-3 and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4 mRNA expression, whereas collagen type I was decreased, and aggrecan, collagen type II as well as MMP-1, -2, -13 and ADAMTS-5 were variably affected.
  • Zymography also showed a TNFalpha-dependent increase in MMP-3 expression, but pre-dominantly in the pro-form.
  • [MeSH-major] Aggrecans / metabolism. Endopeptidases / metabolism. Fibrocartilage / metabolism. Glycosaminoglycans / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cartilage, Articular / metabolism. Cattle. Gene Expression. Gene Expression Profiling. Immunohistochemistry. In Vitro Techniques. Nitrous Oxide / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tissue Inhibitor of Metalloproteinases / metabolism

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  • [Cites] FEBS Lett. 2000 May 19;473(3):275-9 [10818225.001]
  • [Cites] Osteoarthritis Cartilage. 2009 Jun;17(6):754-60 [19121588.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Nov 30;278(3):511-5 [11095942.001]
  • [Cites] J Biol Chem. 2001 Apr 20;276(16):12501-4 [11278243.001]
  • [Cites] FEBS Lett. 2001 Apr 13;494(3):192-5 [11311239.001]
  • [Cites] Biochim Biophys Acta. 2001 May 3;1526(2):147-58 [11325536.001]
  • [Cites] J Orthop Res. 2001 Jul;19(4):729-37 [11518285.001]
  • [Cites] J Orthop Res. 2001 Sep;19(5):802-8 [11562124.001]
  • [Cites] Arthritis Rheum. 2001 Sep;44(9):2078-83 [11592370.001]
  • [Cites] J Orthop Res. 2002 Jan;20(1):92-100 [11853096.001]
  • [Cites] J Biol Chem. 2002 May 3;277(18):16059-66 [11854269.001]
  • [Cites] J Cell Sci. 2002 Oct 1;115(Pt 19):3719-27 [12235282.001]
  • [Cites] Arthritis Rheum. 2003 Jan;48(1):119-33 [12528112.001]
  • [Cites] J Appl Physiol (1985). 2003 Jul;95(1):308-13 [12665533.001]
  • [Cites] J Biol Chem. 2003 Nov 14;278(46):45539-45 [12890681.001]
  • [Cites] FEBS Lett. 2003 Dec 18;555(3):431-6 [14675751.001]
  • [Cites] J Biol Chem. 2004 Mar 5;279(10):8592-601 [14681236.001]
  • [Cites] J Biol Chem. 1991 May 15;266(14):8683-5 [2026585.001]
  • [Cites] Am J Pathol. 1993 Jan;142(1):95-105 [8424468.001]
  • [Cites] Arthritis Rheum. 1993 Feb;36(2):181-9 [8431206.001]
  • [Cites] Anal Biochem. 1993 Dec;215(2):171-9 [8122775.001]
  • [Cites] Arthritis Rheum. 1995 Feb;38(2):164-72 [7848306.001]
  • [Cites] J Biol Chem. 1995 Jun 16;270(24):14313-8 [7782289.001]
  • [Cites] J Biol Chem. 1996 Jan 19;271(3):1544-50 [8576151.001]
  • [Cites] J Bone Joint Surg Am. 1996 Feb;78(2):265-74 [8609118.001]
  • [Cites] J Biol Chem. 1996 Jul 19;271(29):17119-23 [8663332.001]
  • [Cites] Clin Exp Rheumatol. 1996 Mar-Apr;14(2):155-62 [8737721.001]
  • [Cites] Eur J Biochem. 1997 Mar 1;244(2):653-7 [9119036.001]
  • [Cites] J Clin Invest. 1997 Apr 1;99(7):1534-45 [9119997.001]
  • [Cites] Arthritis Rheum. 1998 Apr;41(4):687-93 [9550478.001]
  • [Cites] J Orthop Res. 1998 Jan;16(1):104-11 [9565081.001]
  • [Cites] Curr Opin Rheumatol. 1998 May;10(3):263-8 [9608331.001]
  • [Cites] FEBS Lett. 1998 Sep 11;435(1):39-44 [9755855.001]
  • [Cites] J Biol Chem. 1999 Apr 16;274(16):10846-51 [10196161.001]
  • [Cites] Science. 1999 Jun 4;284(5420):1664-6 [10356395.001]
  • [Cites] Ann N Y Acad Sci. 1999 Jun 30;878:92-107 [10415722.001]
  • [Cites] Arthritis Rheum. 1999 Oct;42(10):2123-31 [10524683.001]
  • [Cites] Connect Tissue Res. 2005;46(2):83-91 [16019418.001]
  • [Cites] Matrix Biol. 2007 May;26(4):259-68 [17174540.001]
  • [Cites] Osteoarthritis Cartilage. 2007 Sep;15(9):1053-60 [17448702.001]
  • [Cites] Arthritis Rheum. 2007 Sep;56(9):3033-42 [17729298.001]
  • [Cites] J Orthop Res. 2008 Apr;26(4):504-12 [18050309.001]
  • [Cites] Osteoarthritis Cartilage. 2008 Oct;16(10):1213-9 [18439846.001]
  • [Cites] Clin Orthop Relat Res. 2009 Jun;467(6):1557-67 [18975039.001]
  • [Cites] Ann Rheum Dis. 2000 Jun;59(6):455-61 [10834863.001]
  • (PMID = 19778432.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aggrecans; 0 / Glycosaminoglycans; 0 / Tissue Inhibitor of Metalloproteinases; 0 / Tumor Necrosis Factor-alpha; EC 3.4.- / Endopeptidases; EC 3.4.99.- / aggrecanase; K50XQU1029 / Nitrous Oxide
  • [Other-IDs] NLM/ PMC2787293
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45. Wang F, Graham WV, Wang Y, Witkowski ED, Schwarz BT, Turner JR: Interferon-gamma and tumor necrosis factor-alpha synergize to induce intestinal epithelial barrier dysfunction by up-regulating myosin light chain kinase expression. Am J Pathol; 2005 Feb;166(2):409-19
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  • [Title] Interferon-gamma and tumor necrosis factor-alpha synergize to induce intestinal epithelial barrier dysfunction by up-regulating myosin light chain kinase expression.
  • Numerous intestinal diseases are characterized by immune cell activation and compromised epithelial barrier function.
  • We have shown that cytokine treatment of epithelial monolayers increases myosin II regulatory light chain (MLC) phosphorylation and decreases barrier function and that these are both reversed by MLC kinase (MLCK) inhibition.
  • The aim of this study was to determine the mechanisms by which interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha regulate MLC phosphorylation and disrupt epithelial barrier function.
  • Barrier dysfunction was also induced by TNF-alpha addition to IFN-gamma-primed, but not control, Caco-2 monolayers.
  • TNF-alpha treatment of IFN-gamma-primed monolayers caused increases in both MLCK expression and MLC phosphorylation, suggesting that MLCK is a TNF-alpha-inducible protein.
  • These effects of TNF-alpha were not mediated by nuclear factor-kappaB.
  • However, at doses below those needed for nuclear factor-kappaB inhibition, sulfasalazine was able to prevent TNF-alpha-induced barrier dysfunction, MLCK up-regulation, and MLC phosphorylation.
  • Low-dose sulfasalazine also prevented morphologically evident tight junction disruption induced by TNF-alpha.
  • These data show that IFN-gamma can prime intestinal epithelial monolayers to respond to TNF-alpha by disrupting tight junction morphology and barrier function via MLCK up-regulation and MLC phosphorylation.
  • These TNF-alpha-induced events can be prevented by the clinically relevant drug sulfasalazine.

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  • [Cites] Am J Physiol. 1997 Oct;273(4 Pt 1):C1378-85 [9357784.001]
  • [Cites] Lancet. 1993 Jun 5;341(8858):1437-9 [8099141.001]
  • [Cites] J Clin Invest. 1998 Mar 1;101(5):1163-74 [9486988.001]
  • [Cites] Gastroenterology. 1998 Apr;114(4):657-68 [9516386.001]
  • [Cites] J Cell Sci. 1999 Jan;112 ( Pt 1):137-46 [9841910.001]
  • [Cites] Gastroenterology. 1999 Mar;116(3):593-601 [10029618.001]
  • [Cites] Eur J Cell Biol. 1999 Jan;78(1):56-66 [10082424.001]
  • [Cites] Gut. 1993 May;34(5):616-20 [8504961.001]
  • [Cites] J Cell Physiol. 1993 Dec;157(3):519-27 [8253863.001]
  • [Cites] Gastroenterology. 1995 Jan;108(1):132-7 [7528696.001]
  • [Cites] Methods Enzymol. 1994;234:555-72 [7808332.001]
  • [Cites] Cytokine. 1995 Jul;7(5):441-8 [7578982.001]
  • [Cites] Epithelial Cell Biol. 1995;4(1):25-34 [8563793.001]
  • [Cites] Am J Physiol. 1996 Nov;271(5 Pt 1):C1678-84 [8944652.001]
  • [Cites] Am J Physiol. 1997 Aug;273(2 Pt 1):G314-21 [9277409.001]
  • [Cites] Am J Physiol. 1999 May;276(5 Pt 1):G1279-88 [10330020.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 25;96(11):6377-81 [10339595.001]
  • [Cites] Am J Physiol. 1999 Sep;277(3 Pt 1):C554-62 [10484342.001]
  • [Cites] Dig Dis Sci. 1999 Nov;44(11):2334-43 [10573384.001]
  • [Cites] J Cell Sci. 2000 May;113 ( Pt 10):1771-81 [10769208.001]
  • [Cites] J Cell Sci. 2000 Jun;113 ( Pt 11):2085-90 [10806119.001]
  • [Cites] Gastroenterology. 2000 Nov;119(5):1209-18 [11054378.001]
  • [Cites] Am J Physiol Cell Physiol. 2000 Dec;279(6):C1918-24 [11078707.001]
  • [Cites] Gastroenterology. 2000 Dec;119(6):1524-36 [11113074.001]
  • [Cites] Gastroenterology. 2000 Dec;119(6):1740-4 [11113095.001]
  • [Cites] Dig Dis Sci. 2000 Nov;45(11):2122-6 [11215725.001]
  • [Cites] Gastroenterology. 2001 May;120(6):1393-403 [11313309.001]
  • [Cites] Int J Colorectal Dis. 2001 Jun;16(3):174-81 [11459291.001]
  • [Cites] Immunology. 2001 Aug;103(4):473-8 [11529938.001]
  • [Cites] J Physiol. 2001 Sep 1;535(Pt 2):541-52 [11533143.001]
  • [Cites] Cytokine. 2001 Aug 21;15(4):212-22 [11563881.001]
  • [Cites] Leukemia. 2001 Oct;15(10):1633-40 [11587223.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2001 Dec;281(6):G1487-93 [11705754.001]
  • [Cites] Curr Biol. 2001 Nov 27;11(23):1847-57 [11728307.001]
  • [Cites] Gastroenterology. 2002 Jul;123(1):163-72 [12105845.001]
  • [Cites] Am J Gastroenterol. 2002 Aug;97(8):2000-4 [12190167.001]
  • [Cites] J Clin Invest. 2002 Dec;110(11):1739-47 [12464679.001]
  • [Cites] Am J Physiol Cell Physiol. 2003 Apr;284(4):C953-61 [12466150.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2003 Apr;284(4):G703-12 [12505880.001]
  • [Cites] Nat Med. 2003 May;9(5):575-81 [12692538.001]
  • [Cites] Gastroenterology. 2003 Sep;125(3):795-804 [12949725.001]
  • [Cites] J Immunol. 2003 Dec 1;171(11):6164-72 [14634132.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Mar;286(3):G367-76 [14766535.001]
  • [Cites] Lab Invest. 2004 Mar;84(3):282-91 [14767487.001]
  • [Cites] J Clin Invest. 1989 Feb;83(2):724-7 [2492310.001]
  • [Cites] J Clin Invest. 1989 Apr;83(4):1089-94 [2649511.001]
  • [Cites] Eur J Pharmacol. 1989 Oct 10;169(2-3):225-34 [2572437.001]
  • [Cites] Cancer Res. 1990 Apr 1;50(7):2172-6 [2180562.001]
  • [Cites] J Membr Biol. 1990 Jun;116(2):177-84 [2380981.001]
  • [Cites] Am J Physiol. 1992 Nov;263(5 Pt 2):F915-24 [1279987.001]
  • [Cites] J Immunol. 1993 Mar 15;150(6):2356-63 [8450217.001]
  • [Cites] Gastroenterology. 1997 Dec;113(6):1873-82 [9394726.001]
  • (PMID = 15681825.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK042086; United States / NIDDK NIH HHS / DK / DK 42086; United States / NCI NIH HHS / CA / CA 14599; United States / NCI NIH HHS / CA / P30 CA014599; United States / NIDDK NIH HHS / DK / R01 DK061931; United States / NIDDK NIH HHS / DK / R01 DK068271; United States / NIDDK NIH HHS / DK / DK 61931
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 3XC8GUZ6CB / Sulfasalazine; 82115-62-6 / Interferon-gamma; EC 2.7.11.18 / Myosin-Light-Chain Kinase
  • [Other-IDs] NLM/ PMC1237049
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46. Fan LF, Dong WG, Jiang CQ, Qian Q, Yu QF: Role of Hypoxia-inducible factor-1 alpha and Survivin in colorectal carcinoma progression. Int J Colorectal Dis; 2008 Nov;23(11):1057-64
MedlinePlus Health Information. consumer health - Colorectal Cancer.

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  • [Title] Role of Hypoxia-inducible factor-1 alpha and Survivin in colorectal carcinoma progression.
  • BACKGROUND AND AIMS: Hypoxia-inducible factor-1 alpha (HIF-1 alpha) is the main active subunit of HIF-1 that promoted tumor cells survival and critical steps in tumor progression and aggressiveness.
  • The authors aimed to investigate the role of HIF-1 alpha and Survivin in colorectal cancer (CRC) progression.
  • MATERIALS AND METHODS: Plasmid expressing small interfering RNA (siRNA) against HIF-1 alpha was constructed and transfected into LS174T cells with Lipofectamine.
  • The inhibitory effects of siRNA on HIF-1 alpha gene was determined by semiquantitative reverse transcriptase polymerase chain reaction and Western blot.
  • Expression of HIF-1 alpha and Survivin was investigated by immunohistochemistry in colorectal adenocarcinomas tissue microarrays.
  • RESULTS: HIF-1 alpha and Survivin expressions were markedly downregulated after the siRNA expression vector against HIF-1 alpha was transfected into the LS174T cells.
  • Of the eight adenoma lesions, one case (12.25%) and four cases (50%) were positive for HIF-1 alpha and Survivin, respectively.
  • Of the 69 cases of CRCs, 46 cases (66.7%) and 39 cases (56.5%) were positive for HIF-1 alpha and Survivin, respectively.
  • The positive rate of HIF-1 alpha protein in CRCs was significantly higher than that in colorectal adenoma lesions (P < 0.05).
  • HIF-1 alpha protein expression was significantly higher in patients with stage III than in patients with stage I-II CRCs (P < 0.01).
  • In addition, overexpression of HIF-1 alpha in higher stages of CRCs was found to correlate positively with Survivin levels (P < 0.001).
  • CONCLUSIONS: Our data demonstrate that HIF-1 alpha and Survivin are mostly expressed in invasive CRCs.
  • Inhibition of HIF-1 alpha may lead to exploration of its potential as a diagnostic tool and possibly a target for gene therapy for colorectal carcinoma.
  • [MeSH-major] Colorectal Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Microtubule-Associated Proteins / genetics. Neoplasm Proteins / genetics. RNA, Neoplasm / genetics
  • [MeSH-minor] Biomarkers, Tumor / biosynthesis. Biomarkers, Tumor / genetics. Blotting, Western. Disease Progression. Humans. Immunohistochemistry. Inhibitor of Apoptosis Proteins. Neoplasm Staging. RNA, Small Interfering / biosynthesis. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] J Cancer Res Clin Oncol. 2005 Aug;131(8):504-10 [15902487.001]
  • [Cites] Gene Ther. 2004 Aug;11(15):1215-23 [15141159.001]
  • [Cites] Am J Pathol. 2003 Sep;163(3):935-46 [12937134.001]
  • [Cites] J Clin Pathol. 2005 Feb;58(2):172-7 [15677538.001]
  • [Cites] Nature. 2006 May 25;441(7092):437-43 [16724055.001]
  • [Cites] J Biol Chem. 1995 Jan 20;270(3):1230-7 [7836384.001]
  • [Cites] Am J Pathol. 2004 Nov;165(5):1489-98 [15509520.001]
  • [Cites] Virchows Arch. 2006 Aug;449(2):164-70 [16810543.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9493-8 [8790358.001]
  • [Cites] World J Gastroenterol. 2003 Mar;9(3):491-4 [12632503.001]
  • [Cites] Pancreas. 2006 Mar;32(2):159-63 [16552335.001]
  • [Cites] World J Gastroenterol. 2005 Aug 14;11(30):4689-92 [16094711.001]
  • [Cites] J Egypt Natl Canc Inst. 2005 Mar;17(1):42-50 [16353082.001]
  • [Cites] Mol Cell Biol. 1992 Dec;12(12):5447-54 [1448077.001]
  • [Cites] Gynecol Oncol. 2007 Jan;104(1):139-44 [16919715.001]
  • [Cites] Cancer Sci. 2005 Mar;96(3):176-82 [15771621.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4881-7 [15930309.001]
  • [Cites] JAMA. 2001 Jan 17;285(3):324-8 [11176843.001]
  • [Cites] J Biol Chem. 2004 Oct 22;279(43):44976-86 [15322093.001]
  • [Cites] Eur J Cancer. 2006 Nov;42(17):2996-3003 [16996732.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6130-4 [14559790.001]
  • [Cites] FEBS Lett. 2001 Dec 7;509(2):225-9 [11741593.001]
  • [Cites] Chin Med J (Engl). 2004 Oct;117(10):1541-6 [15498380.001]
  • [Cites] Clin Cancer Res. 2000 Jan;6(1):127-34 [10656440.001]
  • [Cites] J Biol Chem. 2006 Sep 8;281(36):25903-14 [16847054.001]
  • [Cites] Biomed Pharmacother. 2006 Jul;60(6):289-92 [16876381.001]
  • [Cites] Int J Cancer. 2004 Oct 10;111(6):849-57 [15300796.001]
  • [Cites] Nat Rev Cancer. 2003 Jan;3(1):46-54 [12509766.001]
  • [Cites] Pancreas. 2006 Apr;32(3):297-305 [16628086.001]
  • (PMID = 18704463.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering
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47. Shah SJ, Blumen S, Pitha-Rowe I, Kitareewan S, Freemantle SJ, Feng Q, Dmitrovsky E: UBE1L represses PML/RAR{alpha} by targeting the PML domain for ISG15ylation. Mol Cancer Ther; 2008 Apr;7(4):905-14
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  • [Title] UBE1L represses PML/RAR{alpha} by targeting the PML domain for ISG15ylation.
  • Acute promyelocytic leukemia (APL) is characterized by expression of promyelocytic leukemia (PML)/retinoic acid (RA) receptor alpha (RARalpha) protein and all-trans-RA-mediated clinical remissions.

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  • [Cites] Cancer Res. 2004 Nov 1;64(21):8109-15 [15520223.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2244-51 [9746761.001]
  • [Cites] EMBO J. 2001 Feb 1;20(3):362-71 [11157743.001]
  • [Cites] J Exp Med. 2001 Jun 18;193(12):1361-71 [11413191.001]
  • [Cites] J Biol Chem. 2002 Mar 22;277(12):9976-81 [11788588.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3806-11 [11891284.001]
  • [Cites] J Clin Oncol. 2005 Jul 20;23(21):4776-89 [16034054.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Aug;6(8):599-609 [16064136.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):921-8 [16424026.001]
  • [Cites] J Biol Chem. 2006 Feb 17;281(7):3989-94 [16352599.001]
  • [Cites] Blood Cells Mol Dis. 2006 May-Jun;36(3):406-13 [16647867.001]
  • [Cites] EMBO J. 2006 Jun 7;25(11):2358-67 [16710296.001]
  • [Cites] Oncogene. 2007 Aug 2;26(35):5098-106 [17310991.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1723-30 [12970771.001]
  • [Cites] Gene. 2002 May 29;291(1-2):17-27 [12095675.001]
  • [Cites] J Biol Chem. 2003 Jan 17;278(3):1594-602 [12426315.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7305-15 [14576840.001]
  • [Cites] Clin Cancer Res. 2004 Apr 1;10(7):2570-7 [15073138.001]
  • [Cites] J Biol Chem. 2004 Apr 30;279(18):18178-87 [14976209.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 18;101(20):7578-82 [15131269.001]
  • [Cites] Sci STKE. 2004 Aug 10;2004(245):pe43 [15304665.001]
  • [Cites] N Engl J Med. 1991 May 16;324(20):1385-93 [1850498.001]
  • [Cites] Cell. 1991 Aug 23;66(4):663-74 [1652368.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2694-8 [1372989.001]
  • [Cites] Oncology (Williston Park). 1992 Aug;6(8):74-78, 83; discussion 84, 87-8 [1323988.001]
  • [Cites] Am J Pathol. 1993 Nov;143(5):1301-11 [8238249.001]
  • [Cites] Cancer Res. 1996 Jul 1;56(13):2945-8 [8674046.001]
  • [Cites] Blood. 1996 Nov 15;88(10):3926-36 [8916959.001]
  • [Cites] J Biol Chem. 1998 Feb 6;273(6):3117-20 [9452416.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14807-12 [10611294.001]
  • (PMID = 18413804.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA062275-13; United States / NCI NIH HHS / CA / R01-CA087546; United States / NCI NIH HHS / CA / R01 CA062275-08; United States / NCI NIH HHS / CA / CA087546-08; United States / NCI NIH HHS / CA / R01 CA087546-02; United States / NCI NIH HHS / CA / CA087546-03; United States / NCI NIH HHS / CA / R01 CA111422; United States / NCI NIH HHS / CA / CA111422-01A1; United States / NCI NIH HHS / CA / CA062275-10; United States / NCI NIH HHS / CA / CA087546-07; United States / NCI NIH HHS / CA / R01 CA087546-04; United States / NCI NIH HHS / CA / R01 CA111422-02; United States / NCI NIH HHS / CA / R01 CA062275-09; United States / NCI NIH HHS / CA / CA062275-08; United States / NCI NIH HHS / CA / CA062275-11; United States / NCI NIH HHS / CA / R01 CA087546-07; United States / NCI NIH HHS / CA / R01 CA062275; United States / NCI NIH HHS / CA / R01-CA111422; United States / NCI NIH HHS / CA / CA062275-12; United States / NCI NIH HHS / CA / R01 CA062275-13; United States / NCI NIH HHS / CA / CA087546-04; United States / NCI NIH HHS / CA / CA087546-05; United States / NCI NIH HHS / CA / CA111422-02; United States / NCI NIH HHS / CA / CA062275-07; United States / NCI NIH HHS / CA / R01 CA087546-08; United States / NCI NIH HHS / CA / R01 CA087546-05; United States / NCI NIH HHS / CA / R01 CA087546; United States / NCI NIH HHS / CA / R01 CA062275-07; United States / NCI NIH HHS / CA / R01 CA111422-03; United States / NCI NIH HHS / CA / CA111422-04; United States / NCI NIH HHS / CA / R01 CA062275-12; United States / NCI NIH HHS / CA / R01 CA087546-01; United States / NCI NIH HHS / CA / R01 CA087546-06A1; United States / NCI NIH HHS / CA / T32-CA00959; United States / NCI NIH HHS / CA / CA087546-06A1; United States / NCI NIH HHS / CA / CA062275-09; United States / NCI NIH HHS / CA / R01 CA062275-10; United States / NCI NIH HHS / CA / CA087546-01; United States / NCI NIH HHS / CA / CA111422-03; United States / NCI NIH HHS / CA / CA087546-02; United States / NCI NIH HHS / CA / R01 CA111422-01A1; United States / NCI NIH HHS / CA / R01 CA111422-04; United States / NCI NIH HHS / CA / R01 CA087546-03; United States / NCI NIH HHS / CA / R01-CA062275; United States / NCI NIH HHS / CA / R01 CA062275-11
  • [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 / Antineoplastic Agents; 0 / Cytokines; 0 / Leupeptins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / Ubiquitins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 110044-82-1 / acetylleucyl-leucyl-norleucinal; 5688UTC01R / Tretinoin; 60267-61-0 / ISG15 protein, human; EC 3.4.- / Endopeptidases; EC 3.4.99.- / USP18 protein, human; EC 6.3.2.19 / Ubiquitin-Activating Enzymes
  • [Other-IDs] NLM/ NIHMS79456; NLM/ PMC2597092
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48. Shiobara N, Suzuki Y, Aoki H, Gotoh A, Fujii Y, Hamada Y, Suzuki S, Fukui N, Kurane I, Itoh T, Suzuki R: Bacterial superantigens and T cell receptor beta-chain-bearing T cells in the immunopathogenesis of ulcerative colitis. Clin Exp Immunol; 2007 Oct;150(1):13-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bacterial superantigens and T cell receptor beta-chain-bearing T cells in the immunopathogenesis of ulcerative colitis.
  • Ulcerative colitis (UC) is a chronic relapsing-remitting inflammatory bowel disease (IBD) that affects the colon and the rectum producing debilitating symptoms, which impair ability to function and quality of life.
  • The aetiology of IBD is incompletely understood, but within the lymphocyte population, specific T cell subsets are known to be major factors in the development of intestinal immune pathology while different subsets are essential regulators, controlling IBD.
  • The percentage of T cell-bearing beta-chain 4 (TCRBV4) was high in patients with UC, and T cells showed polyclonal expansion in the presence of bacterial superantigens (SA) such as streptococcal mitogenic exotoxin Z-2 (SMEZ-2), indicating that bacterial SA promote specific TCRBV family expansion.
  • In conclusion, our observations in this study support the perception that the systemic activation of T cells by enteric bacterial SA might lead to a dysregulated, but exuberant immune activity causing the remission and flare-up cycle of mucosal inflammation in patients with UC.
  • [MeSH-major] Antigens, Bacterial / immunology. Colitis, Ulcerative / immunology. Receptors, Antigen, T-Cell, alpha-beta / analysis. Superantigens / immunology. T-Lymphocyte Subsets / immunology
  • [MeSH-minor] Adolescent. Adult. Bacterial Proteins / immunology. Bacterial Toxins / immunology. Cell Proliferation. Enterotoxins / immunology. Exotoxins / immunology. Female. Genotype. HLA-DR Antigens / genetics. HLA-DRB1 Chains. Humans. Immunity, Mucosal. Intestinal Mucosa / immunology. Lymphocyte Activation / immunology. Male. Middle Aged. Streptolysins / immunology. Time Factors

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  • [Cites] Mol Med Today. 2000 Mar;6(3):125-32 [10689316.001]
  • [Cites] J Immunol. 1994 May 15;152(10):5109-19 [8176227.001]
  • [Cites] J Allergy Clin Immunol. 2000 Jul;106(1 Pt 2):S32-9 [10887331.001]
  • [Cites] Bone Marrow Transplant. 2001 Apr;27(7):731-9 [11360114.001]
  • [Cites] Acta Odontol Scand. 2001 Aug;59(4):235-43 [11570527.001]
  • [Cites] Curr Gastroenterol Rep. 2001 Dec;3(6):455-6 [11696281.001]
  • [Cites] Int J Colorectal Dis. 2002 Jul;17(4):233-7 [12073071.001]
  • [Cites] Eur J Immunol. 2002 Jul;32(7):2084-92 [12115630.001]
  • [Cites] Eur J Immunol. 2003 Jan;33(1):79-84 [12594835.001]
  • [Cites] Pediatr Res. 2003 Mar;53(3):403-10 [12595587.001]
  • [Cites] Novartis Found Symp. 2003;252:92-8; discussion 98-105, 106-14 [14609214.001]
  • [Cites] Inflamm Bowel Dis. 2003 Nov;9(6):380-5 [14671487.001]
  • [Cites] Cell. 2004 Apr 16;117(2):265-77 [15084263.001]
  • [Cites] Int J Med Microbiol. 2004 Apr;293(7-8):529-37 [15149028.001]
  • [Cites] Dig Dis Sci. 2004 Apr;49(4):565-71 [15185858.001]
  • [Cites] Int J Oncol. 2004 Jul;25(1):133-41 [15201998.001]
  • [Cites] J Immunol. 1994 Sep 15;153(6):2807-18 [8077684.001]
  • [Cites] Dig Dis Sci. 1995 Feb;40(2):291-5 [7851192.001]
  • [Cites] Dig Dis Sci. 1995 Apr;40(4):814-8 [7720475.001]
  • [Cites] Clin Immunol Immunopathol. 1995 Oct;77(1):95-106 [7554490.001]
  • [Cites] J Immunol. 1996 Apr 15;156(8):3024-35 [8609425.001]
  • [Cites] Eur J Immunol. 1996 May;26(5):1156-63 [8647181.001]
  • [Cites] Hum Immunol. 1996 Jun-Jul;48(1-2):114-24 [8824580.001]
  • [Cites] Eur J Immunol. 1997 Jan;27(1):17-25 [9021993.001]
  • [Cites] Am J Gastroenterol. 1997 Dec;92(12 Suppl):5S-11S [9395346.001]
  • [Cites] Hum Immunol. 1997 Aug-Sep;56(1-2):57-69 [9455494.001]
  • [Cites] J Pediatr. 1998 Jul;133(1):103-7 [9672520.001]
  • [Cites] Eur J Immunol. 1998 Nov;28(11):3655-63 [9842908.001]
  • [Cites] J Exp Med. 1999 Jan 4;189(1):89-102 [9874566.001]
  • [Cites] Br J Dermatol. 1998 Dec;139 Suppl 53:17-29 [9990409.001]
  • [Cites] Am J Physiol. 1999 Mar;276(3 Pt 1):G613-21 [10070037.001]
  • [Cites] J Immunol. 2004 Dec 15;173(12):7190-9 [15585840.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2005 Mar;288(3):G417-21 [15701620.001]
  • [Cites] Expert Opin Biol Ther. 2005 Apr;5(4):451-62 [15934825.001]
  • [Cites] BMC Gastroenterol. 2005;5:28 [16144553.001]
  • [Cites] J Clin Apher. 2005 Oct;20(3):171-84 [15892107.001]
  • [Cites] Am J Gastroenterol. 2006 Mar;101(3):572-80 [16542294.001]
  • [Cites] J Immunol. 2006 Jun 1;176(11):7104-11 [16709873.001]
  • [Cites] Gut. 2006 Dec;55(12):1760-7 [16648155.001]
  • [Cites] Dig Dis Sci. 2007 Jun;52(6):1427-33 [17394078.001]
  • [Cites] Dig Dis Sci. 2007 Oct;52(10):2725-31 [17404876.001]
  • [Cites] Eur J Immunol. 2004 Sep;34(9):2347-55 [15307167.001]
  • [Cites] Dig Dis Sci. 1980 Mar;25(3):198-204 [7371464.001]
  • [Cites] Surg Gynecol Obstet. 1985 Apr;160(4):295-8 [3983792.001]
  • [Cites] Postgrad Med J. 1985;61 Suppl 1:35-8 [3932991.001]
  • [Cites] J Clin Lab Immunol. 1988 Feb;25(2):63-8 [2897471.001]
  • [Cites] Cell. 1988 Aug 12;54(4):473-84 [2456856.001]
  • [Cites] Nature. 1988 Aug 4;334(6181):395-402 [3043226.001]
  • [Cites] Lancet. 1990 Jul 7;336(8706):16-9 [1973211.001]
  • [Cites] Gut. 1990 Dec;31(12):1365-70 [2101599.001]
  • [Cites] Gastroenterology. 1991 Oct;101(4):1020-30 [1889695.001]
  • [Cites] Science. 1991 Sep 20;253(5026):1411-5 [1716785.001]
  • [Cites] J Exp Med. 1992 Jan 1;175(1):57-63 [1730926.001]
  • [Cites] J Exp Med. 1993 Aug 1;178(2):713-22 [8393480.001]
  • [Cites] Inflamm Bowel Dis. 2000 Feb;6(1):21-33 [10701146.001]
  • (PMID = 17614973.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Bacterial Proteins; 0 / Bacterial Toxins; 0 / Enterotoxins; 0 / Exotoxins; 0 / HLA-DR Antigens; 0 / HLA-DRB1 Chains; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Streptolysins; 0 / Superantigens; 0 / enterotoxin F, Staphylococcal; 0 / mitogenic exotoxin Z protein, Streptococcus; 0 / streptolysin O
  • [Other-IDs] NLM/ PMC2219284
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49. Behling-Kelly E, McClenahan D, Kim KS, Czuprynski CJ: Viable "Haemophilus somnus" induces myosin light-chain kinase-dependent decrease in brain endothelial cell monolayer resistance. Infect Immun; 2007 Sep;75(9):4572-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Viable "Haemophilus somnus" induces myosin light-chain kinase-dependent decrease in brain endothelial cell monolayer resistance.
  • Decreased monolayer TEER was preceded by phosphorylation of the myosin regulatory light chain and was partially dependent on tumor necrosis factor alpha and myosin light-chain kinase but not interleukin-1beta.

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  • [Cites] Lab Invest. 1999 Oct;79(10):1181-99 [10532583.001]
  • [Cites] Infect Immun. 1999 Nov;67(11):5775-83 [10531228.001]
  • [Cites] Am J Pathol. 1999 Dec;155(6):1915-27 [10595922.001]
  • [Cites] Cytokine. 2000 Jan;12(1):21-5 [10623438.001]
  • [Cites] Cell Mol Neurobiol. 2000 Feb;20(1):57-76 [10690502.001]
  • [Cites] Subcell Biochem. 2000;33:47-59 [10804851.001]
  • [Cites] Am J Physiol Cell Physiol. 2000 Jul;279(1):C195-204 [10898731.001]
  • [Cites] J Neurosci. 2000 Nov 1;20(21):8153-9 [11050138.001]
  • [Cites] Brain Res. 2000 Dec 8;885(2):251-61 [11102579.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2004 Apr;286(4):L841-7 [14672924.001]
  • [Cites] Cell Biol Toxicol. 2004 Feb;20(1):1-14 [15119843.001]
  • [Cites] J Submicrosc Cytol Pathol. 2004 Jan;36(1):7-15 [15311669.001]
  • [Cites] Brain Res. 2004 Nov 19;1027(1-2):48-58 [15494156.001]
  • [Cites] J Am Vet Med Assoc. 1966 Jan 15;148(2):162-6 [5950111.001]
  • [Cites] Cornell Vet. 1977 Jul;67(3):327-32 [872592.001]
  • [Cites] Am J Vet Res. 1981 May;42(5):748-54 [7020497.001]
  • [Cites] J Am Vet Med Assoc. 1983 Jun 15;182(12):1390-2 [6348007.001]
  • [Cites] J Neurochem. 1986 Jul;47(1):254-62 [2940339.001]
  • [Cites] Vet Clin North Am Food Anim Pract. 1987 Mar;3(1):61-73 [3552151.001]
  • [Cites] Infect Immun. 1987 Jun;55(6):1381-6 [3570470.001]
  • [Cites] J Exp Med. 1989 Jun 1;169(6):1977-91 [2499653.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jan;87(1):16-20 [2296576.001]
  • [Cites] In Vitro Cell Dev Biol. 1991 Feb;27A(2):113-20 [1826902.001]
  • [Cites] J Comp Pathol. 1991 Oct;105(3):303-12 [1761761.001]
  • [Cites] Infect Immun. 1993 May;61(5):1750-5 [8478064.001]
  • [Cites] J Cell Sci. 1993 Mar;104 ( Pt 3):773-82 [8314872.001]
  • [Cites] J Cell Biol. 1993 Dec;123(6 Pt 2):1777-88 [8276896.001]
  • [Cites] J Cell Biol. 1994 Dec;127(6 Pt 1):1617-26 [7798316.001]
  • [Cites] J Cell Physiol. 1995 Jun;163(3):510-22 [7775594.001]
  • [Cites] J Cell Biol. 1995 Aug;130(3):613-27 [7622562.001]
  • [Cites] Am J Physiol. 1995 Jul;269(1 Pt 1):L99-108 [7631821.001]
  • [Cites] Can J Physiol Pharmacol. 1996 Jul;74(7):787-800 [8946065.001]
  • [Cites] Microb Pathog. 1997 Jan;22(1):13-21 [9032758.001]
  • [Cites] Am J Physiol. 1997 Jan;272(1 Pt 1):L155-70 [9038915.001]
  • [Cites] In Vitro Cell Dev Biol Anim. 1997 Apr;33(4):243-7 [9156338.001]
  • [Cites] Am J Respir Cell Mol Biol. 1997 May;16(5):489-94 [9160829.001]
  • [Cites] J Cell Sci. 1997 Jul;110 ( Pt 14):1603-13 [9247194.001]
  • [Cites] Infect Immun. 2001 Feb;69(2):845-52 [11159977.001]
  • [Cites] Infect Immun. 2001 Mar;69(3):1650-60 [11179340.001]
  • [Cites] J Appl Physiol (1985). 2001 Oct;91(4):1487-500 [11568129.001]
  • [Cites] Neurochem Res. 2002 Mar;27(3):249-52 [11958524.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1334-9 [12149215.001]
  • [Cites] FEMS Microbiol Lett. 2002 Dec 17;217(2):167-72 [12480099.001]
  • [Cites] Proteins. 2003 Feb 1;50(2):213-21 [12486715.001]
  • [Cites] Vascul Pharmacol. 2002 Jun;38(6):323-37 [12529927.001]
  • [Cites] Annu Rev Neurosci. 1999;22:11-28 [10202530.001]
  • [Cites] Life Sci. 1999;64(21):1941-53 [10353592.001]
  • [Cites] J Biol Chem. 1999 Oct 22;274(43):30361-4 [10521411.001]
  • [Cites] J Am Vet Med Assoc. 1956 Nov 1;129(9):417-21 [13366849.001]
  • [Cites] Am J Vet Res. 1960 Mar;21:403-9 [13853365.001]
  • [Cites] Exp Neurol. 2004 Dec;190(2):446-55 [15530883.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Feb 25;327(4):1114-23 [15652512.001]
  • [Cites] Mol Cell Biol. 2005 Jul;25(14):6259-66 [15988034.001]
  • [Cites] Microb Pathog. 2005 Oct;39(4):121-30 [16125894.001]
  • [Cites] Infect Immun. 2005 Dec;73(12):7844-52 [16299274.001]
  • [Cites] Microbiology. 2006 Jan;152(Pt 1):135-42 [16385123.001]
  • [Cites] Cell Biochem Biophys. 2006;44(1):157-69 [16456244.001]
  • [Cites] J Cell Physiol. 2006 Jul;208(1):123-32 [16547974.001]
  • [Cites] J Cell Sci. 2006 May 15;119(Pt 10):2095-106 [16638813.001]
  • [Cites] J Cell Sci. 2006 Jun 1;119(Pt 11):2269-81 [16723733.001]
  • [Cites] Crit Care Med. 2006 Jul;34(7):1947-54 [16715037.001]
  • [Cites] Infect Immun. 2006 Sep;74(9):5311-8 [16926425.001]
  • [Cites] Int J Med Microbiol. 2006 Dec;296(8):553-8 [17010667.001]
  • [Cites] Thromb Haemost. 2007 Oct;98(4):823-30 [17938807.001]
  • [Cites] Infect Immun. 2003 May;71(5):2787-97 [12704153.001]
  • [Cites] Nat Rev Neurosci. 2003 May;4(5):376-85 [12728265.001]
  • [Cites] Neurosci Lett. 2003 Jun 26;344(2):112-6 [12782340.001]
  • [Cites] Brain Res Brain Res Rev. 2003 Jun;42(3):221-42 [12791441.001]
  • [Cites] Infect Immun. 2003 Sep;71(9):5188-93 [12933863.001]
  • [Cites] Shock. 2003 Oct;20(4):363-8 [14501951.001]
  • [Cites] J Neurosci Res. 2003 Oct 15;74(2):255-65 [14515355.001]
  • [Cites] Scand J Infect Dis. 2003;35(9):614-8 [14620144.001]
  • [Cites] Infect Immun. 2004 Mar;72(3):1441-9 [14977949.001]
  • [Cites] Am J Physiol. 1997 Jul;273(1 Pt 1):L217-26 [9252559.001]
  • [Cites] Gastroenterology. 1997 Dec;113(6):1873-82 [9394726.001]
  • [Cites] Am J Physiol. 1997 Dec;273(6 Pt 1):C1859-67 [9435490.001]
  • [Cites] J Immunol. 1998 Nov 15;161(10):5640-6 [9820544.001]
  • [Cites] Infect Immun. 1998 Dec;66(12):5692-7 [9826343.001]
  • [Cites] Infect Immun. 1999 Mar;67(3):1131-8 [10024553.001]
  • [Cites] J Neuropathol Exp Neurol. 1999 Mar;58(3):245-54 [10197816.001]
  • (PMID = 17591789.001).
  • [ISSN] 0019-9567
  • [Journal-full-title] Infection and immunity
  • [ISO-abbreviation] Infect. Immun.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / 1K08 AI057989
  • [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 / Interleukin-1; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.18 / Myosin-Light-Chain Kinase
  • [Other-IDs] NLM/ PMC1951199
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50. Packiam M, Shell DM, Liu SV, Liu YB, McGee DJ, Srivastava R, Seal S, Rest RF: Differential expression and transcriptional analysis of the alpha-2,3-sialyltransferase gene in pathogenic Neisseria spp. Infect Immun; 2006 May;74(5):2637-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression and transcriptional analysis of the alpha-2,3-sialyltransferase gene in pathogenic Neisseria spp.
  • Alpha-2,3-sialyltransferase (Lst) is expressed on the outer membrane of Neisseria gonorrhoeae and Neisseria meningitidis and sialylates surface lipooligosaccharide (LOS), facilitating resistance to complement-mediated killing.
  • We confirmed and expanded upon this observation by showing that extracts of 16 random N. gonorrhoeae isolates contain various amounts of Stase activity, but, on average, 2.2-fold-more Stase activity than extracts of 16 N. meningitidis clinical isolates, representing several serogroups and nongroupable strains.

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  • [Cites] Gene. 1995 Dec 1;166(1):101-4 [8529870.001]
  • [Cites] Infect Immun. 2005 Nov;73(11):7390-7 [16239538.001]
  • [Cites] Med Microbiol Immunol. 1996 Sep;185(2):81-7 [8884739.001]
  • [Cites] Infect Immun. 1996 Nov;64(11):4630-7 [8890217.001]
  • [Cites] Mol Immunol. 1999 Sep-Oct;36(13-14):915-28 [10698346.001]
  • [Cites] J Biol Chem. 2001 Apr 20;276(16):12785-90 [11278878.001]
  • [Cites] FEBS Lett. 2001 Apr 27;495(3):178-83 [11334887.001]
  • [Cites] Infect Immun. 2001 Dec;69(12):7425-36 [11705917.001]
  • [Cites] Gene. 2001 Oct 31;278(1-2):211-22 [11707339.001]
  • [Cites] Infect Immun. 2002 Jan;70(1):407-11 [11748209.001]
  • [Cites] Biochim Biophys Acta. 2002 Jun 7;1576(1-2):39-44 [12031482.001]
  • [Cites] Infect Immun. 2002 Jul;70(7):3744-51 [12065517.001]
  • [Cites] FEBS Lett. 2002 Jul 3;522(1-3):52-8 [12095618.001]
  • [Cites] J Bacteriol. 2002 Nov;184(22):6163-73 [12399486.001]
  • [Cites] Mol Microbiol. 2004 Nov;54(3):731-41 [15491363.001]
  • [Cites] J Bacteriol. 1986 Sep;167(3):1009-15 [3091577.001]
  • [Cites] Infect Immun. 1991 Oct;59(10):3604-9 [1910009.001]
  • [Cites] Infect Immun. 1992 Jan;60(1):39-43 [1729195.001]
  • [Cites] Mol Microbiol. 1992 Sep;6(18):2617-28 [1280317.001]
  • [Cites] Infect Immun. 1993 May;61(5):1657-66 [8478054.001]
  • [Cites] Microb Pathog. 1993 Apr;14(4):307-13 [8326854.001]
  • [Cites] Immunobiology. 1993 Apr;187(3-5):382-402 [8330904.001]
  • [Cites] EMBO J. 1993 Nov;12(11):4043-51 [7693451.001]
  • [Cites] J Bacteriol. 1995 Apr;177(8):1952-8 [7721686.001]
  • [Cites] Microbiology. 1995 Apr;141 ( Pt 4):907-11 [7773394.001]
  • [Cites] Microbiology. 1995 Apr;141 ( Pt 4):913-20 [7539687.001]
  • [Cites] J Biol Chem. 1996 Nov 8;271(45):28271-6 [8910446.001]
  • [Cites] Infect Immun. 1997 Nov;65(11):4436-44 [9353017.001]
  • [Cites] J Exp Med. 1998 Mar 2;187(5):743-52 [9480984.001]
  • [Cites] J Infect Dis. 1999 Jan;179(1):124-35 [9841831.001]
  • [Cites] Infect Immun. 1999 Feb;67(2):954-7 [9916114.001]
  • [Cites] Mol Microbiol. 1999 Aug;33(3):651-8 [10417654.001]
  • [Cites] J Bacteriol. 1963 Jun;85:1274-9 [14047217.001]
  • [Cites] Microb Pathog. 1995 Dec;19(6):379-90 [8852279.001]
  • (PMID = 16622200.001).
  • [ISSN] 0019-9567
  • [Journal-full-title] Infection and immunity
  • [ISO-abbreviation] Infect. Immun.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI033505; United States / NIAID NIH HHS / AI / AI33505
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.4.99.- / Sialyltransferases; EC 2.4.99.4 / beta-galactoside alpha-2,3-sialyltransferase
  • [Other-IDs] NLM/ PMC1459705
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51. Tretter L, Adam-Vizi V: Alpha-ketoglutarate dehydrogenase: a target and generator of oxidative stress. Philos Trans R Soc Lond B Biol Sci; 2005 Dec 29;360(1464):2335-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha-ketoglutarate dehydrogenase: a target and generator of oxidative stress.
  • Alpha-ketoglutarate dehydrogenase (alpha-KGDH) is a highly regulated enzyme, which could determine the metabolic flux through the Krebs cycle.
  • It catalyses the conversion of alpha-ketoglutarate to succinyl-CoA and produces NADH directly providing electrons for the respiratory chain. alpha-KGDH is sensitive to reactive oxygen species (ROS) and inhibition of this enzyme could be critical in the metabolic deficiency induced by oxidative stress.
  • Aconitase in the Krebs cycle is more vulnerable than alpha-KGDH to ROS but as long as alpha-KGDH is functional NADH generation in the Krebs cycle is maintained.
  • NADH supply to the respiratory chain is limited only when alpha-KGDH is also inhibited by ROS.
  • In addition being a key target, alpha-KGDH is able to generate ROS during its catalytic function, which is regulated by the NADH/NAD+ ratio.
  • The pathological relevance of these two features of alpha-KGDH is discussed in this review, particularly in relation to neurodegeneration, as an impaired function of this enzyme has been found to be characteristic for several neurodegenerative diseases.
  • [MeSH-major] Citric Acid Cycle / physiology. Ketoglutarate Dehydrogenase Complex / metabolism. Mitochondria / metabolism. NAD / metabolism. Neurodegenerative Diseases / metabolism. Oxidative Stress / physiology. Reactive Oxygen Species / metabolism

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  • [Cites] Alcohol Clin Exp Res. 1993 Oct;17(5):1084-8 [8279670.001]
  • [Cites] Trends Neurosci. 1993 Nov;16(11):439-44 [7507613.001]
  • [Cites] Ann N Y Acad Sci. 1999;893:79-94 [10672231.001]
  • [Cites] Neurochem Int. 2000 Feb;36(2):97-112 [10676873.001]
  • [Cites] J Neurosci. 2000 Mar 15;20(6):2094-103 [10704483.001]
  • [Cites] J Biol Chem. 2000 May 5;275(18):13441-7 [10788456.001]
  • [Cites] Trends Pharmacol Sci. 2000 Oct;21(10):395-401 [11050320.001]
  • [Cites] J Neurosci. 2000 Dec 15;20(24):8972-9 [11124972.001]
  • [Cites] J Neurochem. 2001 Jan;76(1):302-6 [11146003.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Mar 2;281(3):645-50 [11237706.001]
  • [Cites] Nat Rev Neurosci. 2001 May;2(5):325-34 [11331916.001]
  • [Cites] Neuroscientist. 2004 Feb;10(1):18-25 [14987444.001]
  • [Cites] J Bioenerg Biomembr. 2000 Dec;32(6):609-15 [15254374.001]
  • [Cites] J Neurosci. 2004 Sep 8;24(36):7771-8 [15356188.001]
  • [Cites] J Neurosci. 2004 Sep 8;24(36):7779-88 [15356189.001]
  • [Cites] Biochem J. 1964 Aug;92(2):10C-12C [4284458.001]
  • [Cites] Biochem Biophys Res Commun. 1969 Sep 10;36(6):898-904 [4310146.001]
  • [Cites] Biochem Biophys Res Commun. 1969 Sep 10;36(6):891-7 [5388670.001]
  • [Cites] Biochem J. 1972 Jun;128(1):161-3 [4343661.001]
  • [Cites] Biochem J. 1972 Jul;128(3):617-30 [4404507.001]
  • [Cites] Biochem Biophys Res Commun. 1972 Oct 17;49(2):563-71 [4344895.001]
  • [Cites] FEBS Lett. 1973 Jun 15;33(1):84-7 [4737333.001]
  • [Cites] Biochem J. 1973 Jul;134(3):707-16 [4749271.001]
  • [Cites] J Biol Chem. 1974 Mar 10;249(5):1497-505 [4361738.001]
  • [Cites] J Biol Chem. 1974 Jun 25;249(12):3836-42 [4857981.001]
  • [Cites] FEBS Lett. 1974 May 15;42(1):68-72 [4859511.001]
  • [Cites] Biochem J. 1976 May 15;156(2):435-44 [182149.001]
  • [Cites] Adv Biophys. 1976;:187-227 [797242.001]
  • [Cites] J Neurochem. 1977 Mar;28(3):625-31 [16086.001]
  • [Cites] Arch Biochem Biophys. 1977 Apr 30;180(2):248-57 [195520.001]
  • [Cites] Biochem J. 1978 Dec 15;176(3):899-906 [218557.001]
  • [Cites] Biochem J. 1979 Apr 15;180(1):129-35 [39543.001]
  • [Cites] Biochem J. 1979 Jun 15;180(3):533-44 [39549.001]
  • [Cites] J Biol Chem. 1980 Feb 10;255(3):874-6 [7188697.001]
  • [Cites] FEBS Lett. 1980 Sep 22;119(1):1-8 [7000543.001]
  • [Cites] Biochem J. 1980 Nov 1;191(2):421-7 [6263247.001]
  • [Cites] Biochem J. 1981 Sep 15;198(3):525-33 [6275851.001]
  • [Cites] J Neurochem. 1981 Dec;37(6):1548-56 [6460851.001]
  • [Cites] Eur J Pediatr. 1982 Feb;138(1):32-7 [7075624.001]
  • [Cites] Biochem J. 1981 Dec 15;200(3):701-3 [7342978.001]
  • [Cites] J Neurochem. 1984 Apr;42(4):1153-61 [6699641.001]
  • [Cites] Biochem J. 1984 Feb 15;218(1):139-45 [6712610.001]
  • [Cites] J Biol Chem. 1984 Aug 25;259(16):10232-7 [6469961.001]
  • [Cites] Lancet. 1984 Nov 10;2(8411):1095 [6150163.001]
  • [Cites] Ann Neurol. 1985 May;17(5):444-9 [4004169.001]
  • [Cites] Mol Aspects Med. 1985;8(2):89-193 [3908871.001]
  • [Cites] J Neurochem. 1986 Nov;47(5):1376-86 [3760866.001]
  • [Cites] J Biol Chem. 1987 Sep 5;262(25):12316-22 [3624261.001]
  • [Cites] J Neurochem. 1988 May;50(5):1559-65 [3361310.001]
  • [Cites] Neurosci Lett. 1988 May 26;88(2):233-8 [3380359.001]
  • [Cites] Arch Neurol. 1988 Aug;45(8):836-40 [3395256.001]
  • [Cites] J Clin Invest. 1988 Aug;82(2):476-85 [2841353.001]
  • [Cites] J Neurochem. 1989 Mar;52(3):896-901 [2493071.001]
  • [Cites] Lancet. 1989 Jun 3;1(8649):1269 [2566813.001]
  • [Cites] Ann Neurol. 1989 Dec;26(6):719-23 [2557792.001]
  • [Cites] Biochem J. 1990 Jun 1;268(2):421-8 [2363681.001]
  • [Cites] Stroke. 1990 Jul;21(7):1086-90 [2195717.001]
  • [Cites] Neuropharmacology. 1993 Nov;32(11):1259-66 [7509050.001]
  • [Cites] Ann Neurol. 1994 Feb;35(2):204-10 [8109900.001]
  • [Cites] Ann Neurol. 1994 Mar;35(3):312-8 [8122883.001]
  • [Cites] J Biol Chem. 1994 Sep 9;269(36):22459-62 [8077188.001]
  • [Cites] J Biol Chem. 1994 Nov 4;269(44):27414-20 [7961653.001]
  • [Cites] Free Radic Biol Med. 1991;11(1):81-128 [1937131.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jan 1;89(1):132-6 [1729679.001]
  • [Cites] Biochem J. 1992 Apr 1;283 ( Pt 1):41-50 [1373604.001]
  • [Cites] J Mol Cell Cardiol. 1991 Dec;23(12):1359-74 [1811055.001]
  • [Cites] J Neurochem. 1990 Mar;54(3):823-7 [2154550.001]
  • [Cites] Neurosci Lett. 1990 Feb 16;109(3):247-52 [2330128.001]
  • [Cites] Biochem J. 1990 Apr 15;267(2):527-30 [2185742.001]
  • [Cites] J Neurol Sci. 1990 Apr;96(1):49-57 [2351987.001]
  • [Cites] Exp Neurol. 1995 Feb;131(2):193-202 [7895820.001]
  • [Cites] Ann Thorac Surg. 1995 May;59(5):1316-20 [7733760.001]
  • [Cites] Neurochem Res. 1995 Jan;20(1):87-93 [7739764.001]
  • [Cites] Brain Res. 1995 Feb 13;671(2):181-6 [7743206.001]
  • [Cites] J Neurosci. 1995 May;15(5 Pt 1):3318-27 [7751912.001]
  • [Cites] J Biol Chem. 1995 Jun 2;270(22):13399-405 [7768942.001]
  • [Cites] Am J Physiol. 1995 Jul;269(1 Pt 2):H14-22 [7631842.001]
  • [Cites] Neuroreport. 1995 May 30;6(8):1105-8 [7662887.001]
  • [Cites] Science. 1996 May 17;272(5264):1013-6 [8638123.001]
  • [Cites] Neurodegeneration. 1996 Mar;5(1):27-33 [8731379.001]
  • [Cites] Neuron. 1996 Feb;16(2):345-55 [8789949.001]
  • [Cites] J Neurosci. 1996 Sep 15;16(18):5688-97 [8795624.001]
  • [Cites] Brain Res. 1996 Jul 8;726(1-2):153-9 [8836555.001]
  • [Cites] J Neurophysiol. 1996 Sep;76(3):1611-21 [8890280.001]
  • [Cites] Curr Opin Neurobiol. 1996 Oct;6(5):661-6 [8937831.001]
  • [Cites] J Neurochem. 1997 Jan;68(1):255-64 [8978733.001]
  • [Cites] FEBS Lett. 1997 Oct 13;416(1):15-8 [9369223.001]
  • [Cites] J Neurochem. 1997 Dec;69(6):2529-37 [9375686.001]
  • [Cites] Biochemistry. 1998 Jan 13;37(2):552-7 [9425076.001]
  • [Cites] Biochem Biophys Res Commun. 1998 Aug 19;249(2):512-6 [9712727.001]
  • [Cites] Ann Neurol. 1998 Sep;44(3 Suppl 1):S99-109 [9749580.001]
  • [Cites] Neuroreport. 1998 Aug 24;9(12):2781-3 [9760120.001]
  • [Cites] Ann Neurol. 1998 Oct;44(4):676-81 [9778267.001]
  • [Cites] J Neurochem. 1998 Dec;71(6):2392-400 [9832137.001]
  • [Cites] Biochemistry. 1998 Nov 10;37(45):15835-41 [9843389.001]
  • [Cites] J Biol Chem. 1998 Dec 18;273(51):33972-6 [9852050.001]
  • [Cites] J Neurol Sci. 1998 Nov 26;161(1):47-56 [9879681.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 2;96(5):2414-9 [10051656.001]
  • [Cites] Biochim Biophys Acta. 1999 Feb 9;1410(2):159-70 [10076024.001]
  • [Cites] J Neurochem. 1999 May;72(5):1948-58 [10217272.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):6689-93 [10359773.001]
  • [Cites] J Neurochem. 1999 Jul;73(1):220-8 [10386974.001]
  • [Cites] J Biol Chem. 1955 Apr;213(2):951-67 [14367356.001]
  • [Cites] Science. 1993 Oct 29;262(5134):689-95 [7901908.001]
  • [Cites] J Biol Chem. 2001 Jun 29;276(26):23357-61 [11283020.001]
  • [Cites] J Neurochem. 2001 Oct;79(2):266-77 [11677254.001]
  • [Cites] J Neurochem. 2002 Jan;80(1):91-100 [11796747.001]
  • [Cites] J Mol Neurosci. 2001 Dec;17(3):361-9 [11859932.001]
  • [Cites] J Biol Chem. 2002 Mar 22;277(12):10064-72 [11744691.001]
  • [Cites] J Neurochem. 2002 Mar;80(5):780-7 [11948241.001]
  • [Cites] Arch Biochem Biophys. 2002 Oct 15;406(2):222-8 [12361710.001]
  • [Cites] Eur J Biochem. 2002 Oct;269(20):5004-15 [12383259.001]
  • [Cites] J Neurochem. 2003 Jan;84(1):112-8 [12485407.001]
  • [Cites] Eur J Biochem. 2003 Mar;270(6):1036-42 [12631263.001]
  • [Cites] J Neurochem. 2003 May;85(3):563-70 [12694382.001]
  • [Cites] J Neurochem. 2003 Sep;86(5):1101-7 [12911618.001]
  • [Cites] J Physiol. 2003 Oct 15;552(Pt 2):335-44 [14561818.001]
  • [Cites] Neurochem Res. 2003 Oct;28(10):1575-81 [14570403.001]
  • [Cites] J Biol Chem. 1990 Sep 25;265(27):16330-6 [2168888.001]
  • [Cites] Metab Brain Dis. 1990 Dec;5(4):179-84 [2087217.001]
  • [Cites] J Biochem. 1991 Mar;109(3):450-4 [1652585.001]
  • [Cites] J Biol Chem. 1992 May 5;267(13):8757-63 [1315737.001]
  • [Cites] J Neurochem. 1992 Nov;59(5):1609-23 [1402908.001]
  • [Cites] J Neurochem. 1993 Feb;60(2):588-94 [8380437.001]
  • [Cites] J Biol Chem. 1993 Sep 5;268(25):18532-41 [8395507.001]
  • [Cites] J Neurochem. 1993 Dec;61(6):2007-14 [8245957.001]
  • (PMID = 16321804.001).
  • [ISSN] 0962-8436
  • [Journal-full-title] Philosophical transactions of the Royal Society of London. Series B, Biological sciences
  • [ISO-abbreviation] Philos. Trans. R. Soc. Lond., B, Biol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 0U46U6E8UK / NAD; EC 1.2.4.2 / Ketoglutarate Dehydrogenase Complex
  • [Number-of-references] 127
  • [Other-IDs] NLM/ PMC1569585
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52. Nemo R, Murcia N, Dell KM: Transforming growth factor alpha (TGF-alpha) and other targets of tumor necrosis factor-alpha converting enzyme (TACE) in murine polycystic kidney disease. Pediatr Res; 2005 May;57(5 Pt 1):732-7
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  • [Title] Transforming growth factor alpha (TGF-alpha) and other targets of tumor necrosis factor-alpha converting enzyme (TACE) in murine polycystic kidney disease.
  • Transforming growth factor-alpha (TGF-alpha) is abnormally expressed in autosomal recessive polycystic kidney disease (ARPKD).
  • Tumor necrosis factor-alpha converting enzyme (TACE), a metalloproteinase, mediates TGF-alpha processing.
  • In this study, we sought to determine whether TGF-alpha was an absolute requirement for renal cystogenesis and whether its absence would modulate disease severity or related growth factors/receptors expression.
  • Bpk heterozygotes were bred with TGF-alpha null mice to produce cystic and noncystic offspring with or without TGF-alpha.
  • No significant differences in KW, BW, KW/BW%, or BUN were seen in cystic mice with versus without TGF-alpha.
  • Cystic kidney disease and liver disease histology were similar.
  • AR, EGF, HB-EGF, EGFR, and ErbB4 were abnormally expressed to an equal degree in kidneys of mice with versus without TGF-alpha.
  • Although previous data suggest a critical role of TGF-alpha in murine PKD, these data show that TGF-alpha is not required for renal cyst formation or kidney or liver disease progression.
  • We speculate that the therapeutic effect of WTACE2 could have been due to effects on several TACE targets, including TGF-alpha, AR, and ErbB4, as well as metalloproteinases other than TACE.

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  • [Cites] Pediatr Nephrol. 2001 Jan;16(1):45-50 [11198603.001]
  • [Cites] Kidney Int. 2001 Oct;60(4):1240-8 [11576338.001]
  • [Cites] Am J Physiol Cell Physiol. 2001 Nov;281(5):C1695-705 [11600434.001]
  • [Cites] Exp Neurol. 2001 Nov;172(1):182-8 [11681850.001]
  • [Cites] Gastroenterology. 2002 Jun;122(7):1898-912 [12055597.001]
  • [Cites] Exp Cell Res. 2003 Mar 10;284(1):2-13 [12648462.001]
  • [Cites] Gastroenterology. 2003 Apr;124(4):1020-36 [12671899.001]
  • [Cites] Mamm Genome. 2003 Apr;14(4):242-9 [12682776.001]
  • [Cites] EMBO J. 2003 May 15;22(10):2411-21 [12743035.001]
  • [Cites] Nat Genet. 2003 Aug;34(4):455-9 [12872122.001]
  • [Cites] Kidney Int. 2003 Oct;64(4):1310-9 [12969149.001]
  • [Cites] Kidney Int. 2003 Nov;64(5):1573-9 [14531789.001]
  • [Cites] Kidney Int. 2004 Jun;65(6):2018-29 [15149315.001]
  • [Cites] J Biol Chem. 2004 Jun 4;279(23):24179-88 [15066986.001]
  • [Cites] Mol Cell Biol. 1989 Jul;9(7):2771-8 [2789334.001]
  • [Cites] Dev Biol. 1990 Mar;138(1):225-30 [1968405.001]
  • [Cites] Am J Kidney Dis. 1992 Jan;19(1):22-30 [1739078.001]
  • [Cites] Adv Cancer Res. 1992;58:27-52 [1546559.001]
  • [Cites] Pediatr Nephrol. 1993 Apr;7(2):163-72 [8476712.001]
  • [Cites] Cell. 1993 Apr 23;73(2):249-61 [8477444.001]
  • [Cites] Cell. 1993 Apr 23;73(2):263-78 [8477445.001]
  • [Cites] Biochem Biophys Res Commun. 1993 Oct 29;196(2):892-901 [8240367.001]
  • [Cites] Biochem Biophys Res Commun. 1993 Dec 30;197(3):1083-93 [8280123.001]
  • [Cites] J Lab Clin Med. 1994 Sep;124(3):386-94 [8083581.001]
  • [Cites] Am J Kidney Dis. 1994 Oct;24(4):561-8 [7942810.001]
  • [Cites] J Urol. 1995 Mar;153(3 Pt 1):578-83 [7861486.001]
  • [Cites] Kidney Int. 1995 Feb;47(2):490-9 [7723235.001]
  • [Cites] J Lab Clin Med. 1996 Feb;127(2):214-22 [8636651.001]
  • [Cites] Kidney Int. 1996 Sep;50(3):835-44 [8872958.001]
  • [Cites] Endocrinology. 1996 Dec;137(12):5616-23 [8940392.001]
  • [Cites] Am J Physiol. 1997 Jun;272(6 Pt 1):G1540-9 [9227492.001]
  • [Cites] J Urol. 1998 Jan;159(1):291-6 [9400497.001]
  • [Cites] Science. 1998 Nov 13;282(5392):1281-4 [9812885.001]
  • [Cites] Am J Respir Cell Mol Biol. 1999 May;20(5):924-34 [10226062.001]
  • [Cites] J Biol Chem. 2000 Apr 7;275(14):10379-87 [10744726.001]
  • [Cites] Development. 1999 Jun;126(12):2739-50 [10331984.001]
  • [Cites] Kidney Int. 2000 Jan;57(1):33-40 [10620185.001]
  • [Cites] J Am Soc Nephrol. 2000 Apr;11(4):760-3 [10752536.001]
  • [Cites] Oncogene. 2000 Apr 20;19(17):2129-37 [10815804.001]
  • [Cites] J Biol Chem. 2000 Jun 16;275(24):18297-301 [10748057.001]
  • (PMID = 15774823.001).
  • [ISSN] 0031-3998
  • [Journal-full-title] Pediatric research
  • [ISO-abbreviation] Pediatr. Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK059488; United States / NIDDK NIH HHS / DK / P50 DK057306; United States / NIDDK NIH HHS / DK / K08DK-59488; United States / NIDDK NIH HHS / DK / P50DK-57306
  • [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 / Amphiregulin; 0 / Areg protein, mouse; 0 / EGF Family of Proteins; 0 / Glycoproteins; 0 / Hbegf protein, mouse; 0 / Heparin-binding EGF-like Growth Factor; 0 / Intercellular Signaling Peptides and Proteins; 0 / Transforming Growth Factor alpha; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Erbb4 protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-4; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.- / tumor necrosis factor-alpha convertase
  • [Other-IDs] NLM/ NIHMS5092; NLM/ PMC1570100
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53. Long YM, Chen K, Liu XJ, Xie WR, Wang H: Cell-permeable Tat-NBD peptide attenuates rat pancreatitis and acinus cell inflammation response. World J Gastroenterol; 2009 Feb 7;15(5):561-9
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  • Forty-eight rats from the taurocholate group received an intravenous bolus of 13 mg/kg Tat-NBD (wild-type, WT) peptide, Tat-NBD (mutant-type, MT) peptide, NBD peptide or Tat peptide.
  • Expression of IL-1beta and TNF-alpha mRNA was analyzed using a semi-quantitative reverse-transcript polymerase chain reaction (RT-PCR) method.
  • IL-1beta and TNF-alpha protein in culture medium were detected by enzyme linked immunosorbent assay (ELISA).
  • LPS (10 mg/L) resulted in an increase of IL-1beta mRNA, IL-1beta protein, TNF-alpha mRNA and TNF-alpha protein, whereas significantly inhibitory effects were observed when cells were incubated with Tat-NBD (WT).
  • [MeSH-minor] Amino Acid Sequence. Amino Acid Substitution. Animals. Cell Line. Interleukin-1beta / genetics. NF-kappa B / physiology. Peptide Fragments / genetics. Peptide Fragments / therapeutic use. RNA, Messenger / genetics. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction. Taurocholic Acid / toxicity. Tumor Necrosis Factor-alpha / genetics

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  • [Cites] J Am Coll Surg. 2002 Oct;195(4):497-505 [12375755.001]
  • [Cites] J Pathol. 2007 Nov;213(3):239-48 [17893879.001]
  • [Cites] Trends Pharmacol Sci. 2000 Feb;21(2):45-8 [10664605.001]
  • [Cites] Science. 2000 Sep 1;289(5484):1550-4 [10968790.001]
  • [Cites] J Clin Invest. 2001 Jan;107(1):7-11 [11134171.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2001 Jun;280(6):G1197-208 [11352813.001]
  • [Cites] Gastroenterology. 2002 Feb;122(2):448-57 [11832459.001]
  • [Cites] J Biol Chem. 2002 Nov 29;277(48):45992-6000 [12244103.001]
  • [Cites] Gut. 2003 Feb;52(2):270-4 [12524412.001]
  • [Cites] J Biol Chem. 2003 Sep 19;278(38):36676-87 [12867423.001]
  • [Cites] Trends Immunol. 2004 Jun;25(6):280-8 [15145317.001]
  • [Cites] J Biol Chem. 2004 Sep 3;279(36):37219-22 [15252035.001]
  • [Cites] Scand J Gastroenterol. 1980;15(4):411-6 [7433903.001]
  • [Cites] Cell. 1986 Aug 29;46(5):705-16 [3091258.001]
  • [Cites] Pathol Res Pract. 1989 May;184(5):507-13 [2748464.001]
  • [Cites] Yale J Biol Med. 1992 Sep-Oct;65(5):449-56; discussion 465-9 [1340062.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jan 18;91(2):664-8 [8290579.001]
  • [Cites] Am J Clin Pathol. 1996 May;105(5):589-98 [8623768.001]
  • [Cites] Crit Care Med. 1999 Apr;27(4):749-55 [10321665.001]
  • [Cites] World J Gastroenterol. 2005 Jul 21;11(27):4277-80 [16015706.001]
  • [Cites] Shock. 2005 Dec;24 Suppl 1:45-51 [16374372.001]
  • [Cites] Am J Respir Cell Mol Biol. 2006 Aug;35(2):198-205 [16574946.001]
  • [Cites] Ann Rheum Dis. 2006 Nov;65 Suppl 3:iii75-82 [17038479.001]
  • [Cites] Methods Mol Biol. 2000;130:235-46 [10589435.001]
  • (PMID = 19195057.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Gene Products, tat; 0 / Interleukin-1beta; 0 / NF-kappa B; 0 / Peptide Fragments; 0 / Peptides; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 5E090O0G3Z / Taurocholic Acid
  • [Other-IDs] NLM/ PMC2653342
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54. Kawaratani H, Tsujimoto T, Kitazawa T, Kitade M, Yoshiji H, Uemura M, Fukui H: Innate immune reactivity of the liver in rats fed a choline-deficient L-amino-acid-defined diet. World J Gastroenterol; 2008 Nov 21;14(43):6655-61

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIM: To investigate the innate immune reactivity of tumor necrosis factor-alpha (TNF-alpha), Toll-like receptor 4 (TLR4), and CD14 in the liver of non-alcoholic steatohepatitis (NASH) model rats.
  • The liver specimens were immunostained for TNF-alpha, TLR4, and CD14.
  • The gene expressions of TNF-alpha, TLR4, and CD14 were determined by reverse-transcriptase polymerase chain reaction (RT-PCR).
  • Kupffer cells were isolated from the liver by Percoll gradient centrifugation, and were then cultured to measure TNF-alpha production.
  • RESULTS: The serum and liver levels of TNF-alpha in the CDAA-fed rats increased significantly as compared with the control group, as did the immunohistochemical values and gene expressions of TNF-alpha, TLR4, and CD14 with the progression of steatohepatitis.
  • TNF-alpha production from the isolated Kupffer cells of the CDAA-fed rats was elevated by lipopolysaccharide stimulation.
  • CONCLUSION: The expressions of TNF-alpha, TLR4, and CD14 increased in the NASH model, suggesting that TLR4 and CD14-mediated endotoxin liver damage may also occur in NASH.
  • [MeSH-minor] Alanine Transaminase / blood. Animals. Antigens, CD14 / metabolism. Cells, Cultured. Disease Models, Animal. Kupffer Cells / metabolism. Kupffer Cells / pathology. Male. Rats. Rats, Inbred F344. Toll-Like Receptor 4 / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • [Cites] Gastroenterology. 2002 Jul;123(1):134-40 [12105842.001]
  • [Cites] Hepatology. 2001 Dec;34(6):1158-63 [11732005.001]
  • [Cites] Exp Biol Med (Maywood). 2003 Sep;228(8):882-90 [12968059.001]
  • [Cites] Exp Cell Res. 1973 Dec;82(2):391-8 [4358115.001]
  • [Cites] Mayo Clin Proc. 1980 Jul;55(7):434-8 [7382552.001]
  • [Cites] Hepatology. 1994 Aug;20(2):461-74 [8045508.001]
  • [Cites] Carcinogenesis. 1994 Oct;15(10):2201-6 [7955054.001]
  • [Cites] Immunity. 1996 Apr;4(4):407-14 [8612135.001]
  • [Cites] Nature. 1997 Jul 24;388(6640):394-7 [9237759.001]
  • [Cites] Gastroenterology. 1998 Apr;114(4):842-5 [9547102.001]
  • [Cites] J Gastroenterol Hepatol. 1998 Aug;13(8):842-5 [9736181.001]
  • [Cites] Am J Physiol. 1999 Jan;276(1 Pt 1):G98-G106 [9886984.001]
  • [Cites] J Biol Chem. 1999 Apr 16;274(16):10689-92 [10196138.001]
  • [Cites] J Immunol. 1999 Apr 1;162(7):3749-52 [10201887.001]
  • [Cites] Gastroenterology. 1999 Jun;116(6):1413-9 [10348825.001]
  • [Cites] Am J Gastroenterol. 1999 Sep;94(9):2467-74 [10484010.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2005 Jan;288(1):G1-6 [15591584.001]
  • [Cites] Nat Med. 2005 Feb;11(2):183-90 [15685173.001]
  • [Cites] Gut. 2006 Mar;55(3):415-24 [16174657.001]
  • [Cites] Liver Int. 2006 Dec;26(10):1175-86 [17105582.001]
  • [Cites] J Gastroenterol Hepatol. 2007 Jun;22(6):862-9 [17504260.001]
  • [Cites] J Hepatol. 2007 Oct;47(4):571-9 [17644211.001]
  • [Cites] World J Gastroenterol. 2008 Oct 21;14(39):6036-43 [18932283.001]
  • [Cites] Nature. 2000 Aug 17;406(6797):782-7 [10963608.001]
  • [Cites] Int J Oncol. 2001 Jan;18(1):41-7 [11115537.001]
  • [Cites] Semin Liver Dis. 2001;21(1):89-104 [11296700.001]
  • [Cites] Hepatology. 2001 Jul;34(1):101-8 [11431739.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2002 Aug;283(2):G256-65 [12121871.001]
  • (PMID = 19034968.001).
  • [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 / Amino Acids; 0 / Antigens, CD14; 0 / Tlr4 protein, rat; 0 / Toll-Like Receptor 4; 0 / Tumor Necrosis Factor-alpha; EC 2.6.1.2 / Alanine Transaminase
  • [Other-IDs] NLM/ PMC2773307
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55. Matsuda R, Koide T, Tokoro C, Yamamoto T, Godai T, Morohashi T, Fujita Y, Takahashi D, Kawana I, Suzuki S, Umemura S: Quantitive cytokine mRNA expression profiles in the colonic mucosa of patients with steroid naïve ulcerative colitis during active and quiescent disease. Inflamm Bowel Dis; 2009 Mar;15(3):328-34
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] Quantitive cytokine mRNA expression profiles in the colonic mucosa of patients with steroid naïve ulcerative colitis during active and quiescent disease.
  • BACKGROUND: Cytokines have validated roles in the immunopathogenesis of inflammatory bowel disease (IBD).
  • This study was to investigate the expressions of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-8, and IL-10 mRNAs in the colonic mucosa of patients with ulcerative colitis (UC) during active and quiescent UC.
  • Quantitative cytokine mRNA expressions in biopsies were measured by real-time polymerase chain reaction (PCR).
  • At baseline, IL-6, IL-8, TNF-alpha, and IL-10 mRNAs were high in inflamed mucosa compared with NCC (P < 0.01).
  • Both TNF-alpha mRNA (P = 0.03) and IL-6 mRNA (P = 0.04) were higher in UC compared with ICC.
  • Even in non-inflamed mucosa, IL-8 and TNF-alpha mRNA expressions were high compared with NCC.
  • IL-8 mRNA was high even at sites of endoscopically quiescent UC during active disease.
  • [MeSH-minor] Administration, Oral. Adult. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Biopsy. Colonoscopy. Dose-Response Relationship, Drug. Female. Follow-Up Studies. Granulocytes. Humans. Interleukin-6 / biosynthesis. Interleukin-6 / genetics. Interleukin-8 / biosynthesis. Interleukin-8 / genetics. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Leukapheresis / methods. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Remission Induction / methods. Retrospective Studies. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / genetics. Young Adult

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  • [CommentIn] Inflamm Bowel Dis. 2010 May;16(5):734 [19653287.001]
  • (PMID = 18942752.001).
  • [ISSN] 1536-4844
  • [Journal-full-title] Inflammatory bowel diseases
  • [ISO-abbreviation] Inflamm. Bowel Dis.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cytokines; 0 / Interleukin-6; 0 / Interleukin-8; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 4Q81I59GXC / Mesalamine
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56. Kim K, Park U, Wang J, Lee J, Park S, Kim S, Choi D, Kim C, Park J: Gene profiling of colonic serrated adenomas by using oligonucleotide microarray. Int J Colorectal Dis; 2008 Jun;23(6):569-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Three genes were further investigated by means of quantitative reverse transcription polymerase chain reaction (RT-PCR) for validation.
  • [MeSH-minor] Aged. Colonic Polyps / genetics. Female. Humans. Male. Middle Aged. Myelin and Lymphocyte-Associated Proteolipid Proteins. Oligonucleotide Array Sequence Analysis. Receptors, TNF-Related Apoptosis-Inducing Ligand. Retinoic Acid Receptor alpha. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] J Pathol. 2001 Mar;193(3):283-5 [11241405.001]
  • [Cites] Microsc Res Tech. 2000 Aug 1;50(3):184-95 [10891884.001]
  • [Cites] Gastroenterology. 1991 Apr;100(4):1142-3 [2001817.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3544-9 [11325815.001]
  • [Cites] Dis Colon Rectum. 2005 Dec;48(12):2238-48 [16228831.001]
  • [Cites] Gut. 1992 Apr;33(4):518-23 [1582597.001]
  • [Cites] Gastroenterology. 2002 Sep;123(3):862-76 [12198712.001]
  • [Cites] Cancer. 2002 Feb 15;94(4):929-33 [11920460.001]
  • [Cites] Cancer Res. 2002 Aug 1;62(15):4352-63 [12154040.001]
  • [Cites] Mod Pathol. 2005 Feb;18(2):170-8 [15389252.001]
  • [Cites] J Surg Oncol. 2001 Jan;76(1):63-8; discussion 69 [11223827.001]
  • [Cites] J Gastroenterol. 2002;37(6):467-70 [12108682.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Dec 14;289(4):876-81 [11735128.001]
  • [Cites] J Biol Chem. 2001 Jun 22;276(25):23009-17 [11294831.001]
  • [Cites] Cancer Res. 1998 Aug 1;58(15):3391-400 [9699671.001]
  • [Cites] Cancer Res. 2003 Aug 15;63(16):4878-81 [12941809.001]
  • [Cites] Oncogene. 2004 Feb 19;23(7):1377-91 [14973550.001]
  • [Cites] Pathol Int. 2003 May;53(5):277-83 [12713561.001]
  • [Cites] J Clin Pathol. 1999 Jun;52(6):455-60 [10562815.001]
  • [Cites] Science. 1998 Nov 13;282(5392):1318-21 [9812896.001]
  • [Cites] Am J Surg Pathol. 1997 Apr;21(4):417-23 [9130988.001]
  • [Cites] Cell. 1997 Oct 17;91(2):231-41 [9346240.001]
  • [Cites] Methods Mol Med. 2003;71:135-46 [12374018.001]
  • [Cites] Gut. 1997 May;40(5):660-3 [9203947.001]
  • [Cites] Gut. 2004 Aug;53(8):1137-44 [15247181.001]
  • [Cites] Nat Clin Pract Oncol. 2005 Aug;2(8):398-405 [16130936.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Cancer Res. 2003 Oct 15;63(20):6571-4 [14583447.001]
  • [Cites] J Cell Biochem. 2000 Apr;77(4):604-14 [10771516.001]
  • [Cites] Cell. 1993 Dec 17;75(6):1169-78 [7505205.001]
  • [Cites] Gastroenterology. 2000 Aug;119(2):323-32 [10930367.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Aug 3;285(5):1244-9 [11478790.001]
  • [Cites] Dis Colon Rectum. 2004 Feb;47(2):141-52 [15043283.001]
  • [Cites] Gut. 2000 Jul;47(1):43-9 [10861263.001]
  • [Cites] Dis Colon Rectum. 2004 Apr;47(4):481-5 [14994108.001]
  • [Cites] Dis Colon Rectum. 2000 Sep;43(9):1309-13 [11005503.001]
  • [Cites] Am J Gastroenterol. 1989 Feb;84(2):113-7 [2916517.001]
  • [Cites] Genes Dev. 2001 Jan 15;15(2):213-25 [11157777.001]
  • [Cites] Exp Mol Pathol. 2006 Apr;80(2):165-70 [16202996.001]
  • [Cites] Am J Clin Pathol. 2003 Jun;119(6):778-96 [12817424.001]
  • [Cites] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597.001]
  • [Cites] J Clin Pathol. 2004 Jul;57(7):682-6 [15220357.001]
  • [Cites] Gut. 1998 May;42(5):680-4 [9659164.001]
  • [Cites] Oncol Rep. 2004 May;11(5):957-63 [15069532.001]
  • [Cites] J Clin Oncol. 2002 Apr 1;20(7):1932-41 [11919254.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3124-30 [11306497.001]
  • [Cites] Lancet. 1983 Jan 1;1(8314-5):28-30 [6129371.001]
  • [Cites] Ann Oncol. 2004 Dec;15(12):1731-7 [15550577.001]
  • (PMID = 18305945.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / MALL protein, human; 0 / Membrane Proteins; 0 / Myelin and Lymphocyte-Associated Proteolipid Proteins; 0 / RARA protein, human; 0 / Receptors, Retinoic Acid; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Retinoic Acid Receptor alpha; 0 / TNFRSF10A protein, human
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57. Tang YW, Li H, Wu H, Shyr Y, Edwards KM: Host single-nucleotide polymorphisms and altered responses to inactivated influenza vaccine. J Infect Dis; 2007 Oct 1;196(7):1021-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There was no statistical relationship between responses and either tumor necrosis factor- alpha or interleukin (IL)-10 promoter polymorphisms among the 3 response groups.
  • [MeSH-minor] Alleles. Codon. Exons. Gene Frequency. Humans. Influenza A Virus, H1N1 Subtype / immunology. Influenza A Virus, H3N2 Subtype / immunology. Influenza B virus / immunology. Interleukin-10 / genetics. Polymerase Chain Reaction. Polymorphism, Restriction Fragment Length. Promoter Regions, Genetic. Tumor Necrosis Factor-alpha / genetics. Vaccines, Inactivated / administration & dosage. Vaccines, Inactivated / immunology

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  • (PMID = 17763324.001).
  • [ISSN] 0022-1899
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI-52594; United States / NIAID NIH HHS / AI / AI-54174
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / Influenza Vaccines; 0 / Mannose-Binding Lectin; 0 / Tumor Necrosis Factor-alpha; 0 / Vaccines, Inactivated; 130068-27-8 / Interleukin-10
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58. Muñoz LD, Serramía MJ, Fresno M, Muñoz-Fernández MA: Progesterone inhibits HIV-1 replication in human trophoblast cells through inhibition of autocrine tumor necrosis factor secretion. J Infect Dis; 2007 May 1;195(9):1294-302
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  • BACKGROUND: Progesterone levels are higher in placental barriers during pregnancy, but the effect of progesterone on human immunodeficiency virus type 1 (HIV-1) infection in placental cells has not been addressed.
  • Tumor necrosis factor (TNF) messenger RNA was assessed by reverse-transcription polymerase chain reaction (RT-PCR) and quantitative RT-PCR.
  • [MeSH-major] HIV-1 / drug effects. Progesterone / pharmacology. Trophoblasts / secretion. Tumor Necrosis Factor-alpha / biosynthesis. Virus Replication / drug effects
  • [MeSH-minor] DNA Primers. Female. Flow Cytometry. HIV Infections / physiopathology. HIV Long Terminal Repeat / drug effects. Humans. NF-kappa B / drug effects. Pregnancy. Pregnancy Complications, Infectious / physiopathology. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17396998.001).
  • [ISSN] 0022-1899
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 4G7DS2Q64Y / Progesterone
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59. Stefano JT, de Oliveira CP, Corrêa-Giannella ML, de Lima VM, de Sá SV, de Oliveira EP, de Mello ES, Giannella-Neto D, Alves VA, Carrilho FJ: Nonalcoholic steatohepatitis (NASH) in ob/ob mice treated with yo jyo hen shi ko (YHK): effects on peroxisome proliferator-activated receptors (PPARs) and microsomal triglyceride transfer protein (MTP). Dig Dis Sci; 2007 Dec;52(12):3448-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study, we examined the hepatic expression of PPAR-alpha and -gamma and MTP in ob/ob mice receiving or not receiving YHK.
  • PPAR-alpha and -gamma and MTP gene expression was examined by RT-qPCR.
  • YHK promoted an increment in PPAR-alpha and MTP and a decrement in PPAR-gamma mRNA contents.
  • These findings suggest that modulation of PPAR-alpha and -gamma and MTP RNA expression may be implicated in the protective effect of YHK in experimental NASH, limiting hepatocyte lipid accumulation.
  • [MeSH-major] Carrier Proteins / genetics. Fatty Liver / metabolism. Gene Expression / genetics. PPAR alpha / genetics. PPAR gamma / genetics. Plant Preparations / therapeutic use. RNA, Messenger / genetics
  • [MeSH-minor] Animals. Disease Models, Animal. Disease Progression. Hepatocytes / metabolism. Hepatocytes / pathology. Male. Mice. Mice, Obese. Microsomes, Liver. Phytotherapy / methods. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome

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  • (PMID = 17394061.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / PPAR alpha; 0 / PPAR gamma; 0 / Plant Preparations; 0 / RNA, Messenger; 0 / YHK herbal compound; 0 / microsomal triglyceride transfer protein
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60. Abebe F, Mustafa T, Nerland AH, Bjune GA: Cytokine profile during latent and slowly progressive primary tuberculosis: a possible role for interleukin-15 in mediating clinical disease. Clin Exp Immunol; 2006 Jan;143(1):180-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytokine profile during latent and slowly progressive primary tuberculosis: a possible role for interleukin-15 in mediating clinical disease.
  • Using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) we studied the expression levels of interleukin (IL)-2, IL-4, IL-10, IL-12, IL-15, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha during the course of LTB and SPTB in the lungs and spleens of B6D2F1Bom mice infected with the H37Rv strain of Mycobacterium tuberculosis (Mtb).
  • IL-10 and IL-15 increased significantly from phases 2 to 3, whereas that of TNF-alpha decreased significantly and progressively from phases 1 to 3 in the spleens.
  • Over-expression of proinflammatory cytokines during active disease has been well documented, but factor(s) underlying such over-expression is not known.
  • IL-15 is known to up-regulate the production of proinflammatory cytokines, IL-1beta, IL-8, IL-12, IL-17, IFN-gamma and TNF-alpha and has an inhibitory effect on activation-induced cell death.
  • IL-15 is known to be involved in many proinflammatory disease states such as rheumatoid arthritis, sarcoidosis, inflammatory bowel diseases, autoimmune diabetes, etc.
  • Our results, together with the above observations, suggest that IL-15 may play an important role in mediating active disease during Mtb infection.
  • [MeSH-minor] Animals. Disease Progression. Interferon-gamma / genetics. Interleukin-10 / genetics. Interleukin-12 / genetics. Interleukin-15 / genetics. Interleukin-15 / immunology. Interleukin-2 / genetics. Interleukin-4 / genetics. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Models, Animal. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / genetics

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  • [Cites] Scand J Infect Dis. 1998;30(1):59-68 [9670361.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2452-7 [9482906.001]
  • [Cites] Blood. 1998 Dec 15;92(12):4828-35 [9845550.001]
  • [Cites] Eur J Immunol. 1999 Apr;29(4):1265-74 [10229094.001]
  • [Cites] Annu Rev Immunol. 1999;17:19-49 [10358752.001]
  • [Cites] Scand J Immunol. 1999 Aug;50(2):127-36 [10447916.001]
  • [Cites] J Infect Dis. 2000 Jan;181(1):385-9 [10608794.001]
  • [Cites] Infect Immun. 1999 Dec;67(12):6461-72 [10569764.001]
  • [Cites] Clin Exp Immunol. 2005 Aug;141(2):315-25 [15996196.001]
  • [Cites] J Infect Dis. 2000 Mar;181(3):1194-7 [10720554.001]
  • [Cites] J Immunol. 2000 Apr 1;164(7):3608-15 [10725717.001]
  • [Cites] Am J Respir Cell Mol Biol. 2001 Feb;24(2):187-94 [11159053.001]
  • [Cites] Annu Rev Immunol. 2001;19:683-765 [11244051.001]
  • [Cites] Nat Immunol. 2001 Nov;2(11):1054-60 [11600887.001]
  • [Cites] J Allergy Clin Immunol. 2001 Dec;108(6):970-5 [11742275.001]
  • [Cites] Eur J Immunol. 2002 Jun;32(6):1605-13 [12115643.001]
  • [Cites] J Immunol. 2003 Feb 15;170(4):2106-12 [12574382.001]
  • [Cites] Immunology. 2003 Jun;109(2):295-9 [12757625.001]
  • [Cites] Curr Opin Pharmacol. 2004 Aug;4(4):392-7 [15251134.001]
  • [Cites] Clin Exp Immunol. 2004 Oct;138(1):128-38 [15373915.001]
  • [Cites] J Immunol. 1991 May 15;146(10):3444-51 [1827484.001]
  • [Cites] J Immunol. 1993 Jun 1;150(11):4754-65 [7684412.001]
  • [Cites] Science. 1994 May 13;264(5161):965-8 [8178155.001]
  • [Cites] EMBO J. 1994 Jun 15;13(12):2822-30 [8026467.001]
  • [Cites] J Exp Med. 1995 Mar 1;181(3):1255-9 [7869044.001]
  • [Cites] EMBO J. 1995 Aug 1;14(15):3654-63 [7641685.001]
  • [Cites] J Immunol. 1996 Jan 15;156(2):735-41 [8543827.001]
  • [Cites] Nat Med. 1996 Feb;2(2):175-82 [8574962.001]
  • [Cites] J Immunol. 1996 Apr 1;156(7):2413-22 [8786299.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 2;93(7):2897-902 [8610139.001]
  • [Cites] Immunity. 1996 Apr;4(4):329-36 [8612127.001]
  • [Cites] J Clin Invest. 1995 Dec;96(6):2578-82 [8675621.001]
  • [Cites] Am J Respir Crit Care Med. 1997 Mar;155(3):1135-9 [9116999.001]
  • [Cites] J Pathol. 1997 Apr;181(4):444-50 [9196444.001]
  • [Cites] J Immunol. 1997 Sep 15;159(6):3034-43 [9300729.001]
  • [Cites] Eur Respir J. 1997 Sep;10(9):2034-9 [9311498.001]
  • [Cites] Nat Med. 1997 Oct;3(10):1124-8 [9334724.001]
  • [Cites] Blood. 1997 Dec 1;90(11):4513-21 [9373262.001]
  • [Cites] Infect Immun. 1998 Dec;66(12):5743-50 [9826349.001]
  • (PMID = 16367949.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-15; 0 / Interleukin-2; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC1809553
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61. Sachse F, Ahlers F, Stoll W, Rudack C: Neutrophil chemokines in epithelial inflammatory processes of human tonsils. Clin Exp Immunol; 2005 May;140(2):293-300
MedlinePlus Health Information. consumer health - Tonsillitis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Because ELR(+) CXC chemokines are expressed in different types of tonsillitis we investigated the role of the surface/crypt epithelium of human tonsils in producing ELR(+) CXC chemokines: interleukin (IL)-8 (CXCL8), ENA-78 (CXCL5), GRO-alpha (CXCL1) and GCP-2 (CXCL6).
  • Cells were stimulated with tumour necrosis factor (TNF)-alpha, lipopolysaccharide (LPS) and supernatants derived from aerobic/anaerobic Staphylococcus aureus strains.
  • Chemokine expression was measured by quantitative reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA).
  • We observed epithelial expression of IL-8, GRO-alpha and GCP-2 in different types of tonsillitis, whereas ENA-78 was rarely expressed.
  • IL-8 and GCP-2 are expressed in an acute type of tonsillitis whereas GRO-alpha was frequently detectable both in chronically and acutely inflamed tonsils.
  • [MeSH-minor] Adolescent. Adult. Cells, Cultured. Chemokine CXCL1. Chemokine CXCL6. Chemokines, CXC / metabolism. Child. Culture Media, Conditioned. Enzyme-Linked Immunosorbent Assay / methods. Epithelial Cells / immunology. Humans. Intercellular Signaling Peptides and Proteins / metabolism. Interleukin-8 / metabolism. Lipopolysaccharides / immunology. Reverse Transcriptase Polymerase Chain Reaction / methods. Staphylococcus aureus / immunology. Tumor Necrosis Factor-alpha / immunology

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  • [Cites] Immunity. 2000 Feb;12(2):121-7 [10714678.001]
  • [Cites] Immunology. 1994 Sep;83(1):16-24 [7821961.001]
  • [Cites] Acta Otolaryngol Suppl. 2000;543:206-8 [10909021.001]
  • [Cites] J Anat. 2001 Apr;198(Pt 4):497-500 [11327212.001]
  • [Cites] Blood Cells Mol Dis. 2001 Jul-Aug;27(4):728-30 [11778656.001]
  • [Cites] J Anat. 1994 Aug;185 ( Pt 1):111-27 [7559106.001]
  • [Cites] Histochem Cell Biol. 1995 Sep;104(3):211-20 [8542447.001]
  • [Cites] J Immunol. 1997 Apr 15;158(8):3888-94 [9103458.001]
  • [Cites] J Immunol. 1997 Jun 1;158(11):5257-66 [9164944.001]
  • [Cites] Am J Physiol. 1997 Jul;273(1 Pt 1):G75-82 [9252512.001]
  • [Cites] Methods Enzymol. 1997;288:266-97 [9356999.001]
  • [Cites] Pharmacol Rev. 2000 Mar;52(1):145-76 [10699158.001]
  • [Cites] Anat Embryol (Berl). 2001 Nov;204(5):367-73 [11789984.001]
  • [Cites] Allergy. 2002 Dec;57(12):1159-64 [12464044.001]
  • [Cites] Lab Invest. 2003 Jan;83(1):23-34 [12533683.001]
  • [Cites] HNO. 2003 Jun;51(6):480-5 [12835847.001]
  • [Cites] Clin Exp Immunol. 2004 Mar;135(3):511-8 [15008987.001]
  • [Cites] Inflamm Res. 2004 Jan;53(1):4-12 [15021975.001]
  • [Cites] J Exp Med. 1991 Dec 1;174(6):1355-62 [1744577.001]
  • [Cites] J Immunol. 1993 Feb 1;150(3):1000-10 [8423327.001]
  • [Cites] J Biol Chem. 1993 Jul 25;268(21):15419-24 [8340371.001]
  • [Cites] J Leukoc Biol. 2000 Apr;67(4):471-8 [10770278.001]
  • (PMID = 15807854.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CXCL1 protein, human; 0 / CXCL6 protein, human; 0 / Chemokine CXCL1; 0 / Chemokine CXCL6; 0 / Chemokines; 0 / Chemokines, CXC; 0 / Culture Media, Conditioned; 0 / Intercellular Signaling Peptides and Proteins; 0 / Interleukin-8; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC1809351
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62. Fekete K, Decsi T: Long-chain polyunsaturated fatty acids in inborn errors of metabolism. Nutrients; 2010 09;2(9):965-74
Hazardous Substances Data Bank. LINOLEIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-chain polyunsaturated fatty acids in inborn errors of metabolism.
  • This review focuses on the consequences of dietary restriction in IEM on the bioavailability of long-chain polyunsaturated fatty acids (LCPUFAs) and on the attempts to ameliorate these consequences.
  • [MeSH-minor] Adolescent. Adult. Amino Acids / administration & dosage. Arachidonic Acid / administration & dosage. Biological Availability. Child. Child, Preschool. Diet. Diet, Protein-Restricted / adverse effects. Docosahexaenoic Acids / administration & dosage. Humans. Infant. Linoleic Acid / administration & dosage. MEDLINE. Placebos. Randomized Controlled Trials as Topic. alpha-Linolenic Acid / administration & dosage

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  • [Cites] Prostaglandins Leukot Essent Fatty Acids. 2001 Feb;64(2):111-5 [11237478.001]
  • [Cites] Nat Rev Genet. 2006 Jun;7(6):449-60 [16708072.001]
  • [Cites] Indian J Clin Biochem. 2009 Jul;24(3):215-22 [23105838.001]
  • [Cites] Mol Genet Metab. 2006 Jun;88(2):159-65 [16530443.001]
  • [Cites] Pediatr Rev. 2009 Apr;30(4):131-7; quiz 137-8 [19339386.001]
  • [Cites] J Inherit Metab Dis. 1998 Jun;21(4):373-81 [9700594.001]
  • [Cites] J Inherit Metab Dis. 1997 Nov;20(6):783-9 [9427146.001]
  • [Cites] J Inherit Metab Dis. 2007 Jun;30(3):326-32 [17431817.001]
  • [Cites] Arch Dis Child. 2003 Jul;88(7):582-3 [12818902.001]
  • [Cites] J Inherit Metab Dis. 2002 Feb;25(1):56-64 [11999981.001]
  • [Cites] J Inherit Metab Dis. 2006 Apr-Jun;29(2-3):299-303 [16763891.001]
  • [Cites] Am J Clin Nutr. 2003 Sep;78(3 Suppl):640S-646S [12936959.001]
  • [Cites] Prostaglandins Leukot Essent Fatty Acids. 1995 Dec;53(6):401-4 [8821120.001]
  • [Cites] J Inherit Metab Dis. 1994;17(6):704-9 [7707693.001]
  • [Cites] J Inherit Metab Dis. 2010 Dec;33(6):659-64 [20151202.001]
  • [Cites] J Pediatr (Rio J). 2008 Aug;84(4 Suppl):S8-19 [18758655.001]
  • [Cites] J Pediatr. 2000 Oct;137(4):504-9 [11035829.001]
  • [Cites] Dev Med Child Neurol. 2006 Mar;48(3):207-12 [16483397.001]
  • [Cites] Curr Pharm Biotechnol. 2006 Dec;7(6):467-82 [17168664.001]
  • [Cites] Eur J Pediatr. 2000 Oct;159 Suppl 2:S129-35 [11043159.001]
  • [Cites] Prostaglandins Leukot Essent Fatty Acids. 2009 Aug-Sep;81(2-3):159-64 [19615874.001]
  • [Cites] Indian J Pediatr. 2002 May;69(5):421-6 [12061677.001]
  • [Cites] Am Fam Physician. 2006 Jun 1;73(11):1981-90 [16770930.001]
  • [Cites] Acta Paediatr. 2000 Mar;89(3):366-7 [10772290.001]
  • [Cites] Pediatrics. 1998 Dec;102(6):E69 [9832597.001]
  • [Cites] J Pediatr. 1991 Oct;119(4):562-7 [1919887.001]
  • [Cites] J Nutr Biochem. 2000 Nov;11(11-12):543-547 [11137890.001]
  • [Cites] Prostaglandins Leukot Essent Fatty Acids. 2009 Aug-Sep;81(2-3):137-41 [19500961.001]
  • [Cites] Eur J Clin Nutr. 2006 Jul;60(7):915-20 [16523206.001]
  • [Cites] J Inherit Metab Dis. 1997 Nov;20(6):778-82 [9427145.001]
  • [Cites] J Inherit Metab Dis. 2010 Apr;33(2):121-7 [20217236.001]
  • [Cites] Mol Cell Biochem. 1997 Mar;168(1-2):101-15 [9062899.001]
  • [Cites] J Inherit Metab Dis. 2006 Feb;29(1):58-63 [16601869.001]
  • [Cites] J Pediatr Gastroenterol Nutr. 2001 Sep;33(3):253-9 [11593118.001]
  • (PMID = 22254065.001).
  • [ISSN] 2072-6643
  • [Journal-full-title] Nutrients
  • [ISO-abbreviation] Nutrients
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Fatty Acids, Unsaturated; 0 / Placebos; 0RBV727H71 / alpha-Linolenic Acid; 25167-62-8 / Docosahexaenoic Acids; 27YG812J1I / Arachidonic Acid; 9KJL21T0QJ / Linoleic Acid
  • [Keywords] NOTNLM ; alpha-linolenic acid (major topic) / arachidonic acid (major topic) / docosahexaenoic acid (major topic) / inborn errors of metabolism (major topic) / linoleic acid (major topic) / long-chain polyunsaturated fatty acids (major topic)
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63. Gureviciene I, Gurevicius K, Tanila H: Role of alpha-synuclein in synaptic glutamate release. Neurobiol Dis; 2007 Oct;28(1):83-9
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of alpha-synuclein in synaptic glutamate release.
  • Defective mobilization of dopamine from the reserve pool has been reported in both alpha-synuclein knockout mice (KO) and pPrp-A30P transgenic mice.
  • Standard hippocampal slices were prepared from KO, pPrp-A30P, and C57BL/6J wild type (WT1) mice, as well as from mice with transgenic overexpression of wild type human alpha-synuclein (pSyn-hASY) and their negative littermates (WT2), and field responses were measured in CA3 in response to mossy fiber stimulation.
  • Paired-pulse facilitation was significantly weaker in both transgenic alpha-synuclein lines and KO mice compared to their controls.
  • These findings support the idea that lack of alpha-synuclein impairs mobilization of glutamate from the reserve pool.
  • However, transgenic expression of A30P mutated or wild type alpha-synuclein does not appear to prevent endogenous mouse alpha-synuclein to carry out this function.
  • [MeSH-major] Glutamic Acid / secretion. Mossy Fibers, Hippocampal / metabolism. Neuronal Plasticity / physiology. Synapses / metabolism. alpha-Synuclein / metabolism
  • [MeSH-minor] Animals. Excitatory Postsynaptic Potentials / physiology. Humans. Immunohistochemistry. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Transgenic. Mutation. Organ Culture Techniques. Patch-Clamp Techniques. Polymerase Chain Reaction. Promoter Regions, Genetic. Synaptic Transmission / physiology


64. Freudenreich O, Brockman MA, Henderson DC, Evins AE, Fan X, Walsh JP, Goff DC: Analysis of peripheral immune activation in schizophrenia using quantitative reverse-transcription polymerase chain reaction (RT-PCR). Psychiatry Res; 2010 Apr 30;176(2-3):99-102
MedlinePlus Health Information. consumer health - Schizophrenia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of peripheral immune activation in schizophrenia using quantitative reverse-transcription polymerase chain reaction (RT-PCR).
  • Immune system abnormalities in schizophrenia include a shift from a Type 1 (cellular) to a Type 2 (humoral) immune response.
  • To characterize the activation status of the immune system in schizophrenia, we examined the pattern of gene expression in peripheral blood cells for three Th1 cytokines (interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-2 (IL-2)), and one Th2 cytokine (interleukin-10 (IL-10)).
  • In a cross-sectional study, we used quantitative reverse-transcription polymerase chain reaction (RT-PCR) to compare the mRNA levels of IFN-gamma, TNF-alpha, IL-2, and IL-10 in peripheral blood mononuclear cells (PBMCs) between 15 schizophrenia patients and 15 matched healthy controls.
  • Expression of IFN-gamma and TNF-alpha was significantly reduced in patients with schizophrenia compared with normal controls.
  • These results are consistent with impaired Type 1 cellular immunity in schizophrenia.

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  • [Copyright] Copyright (c) 2008 Elsevier Ireland Ltd. All rights reserved.
  • [Cites] Annu Rev Immunol. 2001;19:683-765 [11244051.001]
  • [Cites] J Psychiatr Res. 2000 Nov-Dec;34(6):369-82 [11165304.001]
  • [Cites] Prog Neuropsychopharmacol Biol Psychiatry. 2002 Jan;26(1):33-9 [11853116.001]
  • [Cites] Int J Neurosci. 2001;111(1-2):11-9 [11913333.001]
  • [Cites] Am J Psychiatry. 2002 Jun;159(6):1029-34 [12042193.001]
  • [Cites] J Clin Psychiatry. 2004 Jul;65(7):940-7 [15291683.001]
  • [Cites] Schizophr Bull. 1987;13(2):261-76 [3616518.001]
  • [Cites] Nature. 1987 Dec 17-23;330(6149):662-4 [3317066.001]
  • [Cites] Science. 1988 May 27;240(4856):1169-76 [3131876.001]
  • [Cites] J Exp Med. 1993 Oct 1;178(4):1435-40 [8376946.001]
  • [Cites] Immunol Today. 1996 Mar;17(3):138-46 [8820272.001]
  • [Cites] J Exp Med. 1997 Nov 3;186(9):1591-6 [9348317.001]
  • [Cites] Ann Rheum Dis. 1999 Sep;58(9):585-7 [10460194.001]
  • [Cites] Immunol Rev. 2004 Dec;202:223-36 [15546396.001]
  • [Cites] Prog Neuropsychopharmacol Biol Psychiatry. 2004 Nov;28(7):1129-34 [15610925.001]
  • [Cites] Am J Med Genet B Neuropsychiatr Genet. 2006 Apr 5;141B(3):261-8 [16526044.001]
  • [Cites] J Psychiatr Res. 2007 Jan-Feb;41(1-2):3-7 [16434055.001]
  • [Cites] Int Clin Psychopharmacol. 2007 Jan;22(1):21-7 [17159456.001]
  • [Cites] Schizophr Res. 2007 Feb;90(1-3):179-85 [17208413.001]
  • [Cites] Nervenarzt. 2007 Mar;78(3):253-6, 258-60, 262-3 [16897051.001]
  • [Cites] Arch Gen Psychiatry. 2007 May;64(5):555-64 [17485607.001]
  • [Cites] Schizophr Bull. 2007 May;33(3):729-36 [17085743.001]
  • [Cites] Neuropsychobiology. 2007;56(2-3):55-63 [18037815.001]
  • [Cites] Immunol Rev. 2008 Jun;223:114-31 [18613832.001]
  • [Cites] Schizophr Bull. 1999;25(4):625-38 [10667736.001]
  • [Cites] Mol Psychiatry. 2000 Mar;5(2):150-8 [10822342.001]
  • [Cites] Neuroreport. 2000 Oct 20;11(15):3385-8 [11059907.001]
  • [Cites] Ann N Y Acad Sci. 2000;917:456-67 [11268373.001]
  • (PMID = 20132993.001).
  • [ISSN] 0165-1781
  • [Journal-full-title] Psychiatry research
  • [ISO-abbreviation] Psychiatry Res
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / K24 MH002025; United States / NIMH NIH HHS / MH / MH002025-06; United States / NIMH NIH HHS / MH / K24 MH002025-06
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cytokines
  • [Other-IDs] NLM/ NIHMS178210; NLM/ PMC2844464
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65. Ha TS, Hong EJ, Ahn EM, Ahn HY: Regulation of type IV collagen alpha chains of glomerular epithelial cells in diabetic conditions. J Korean Med Sci; 2009 Oct;24(5):837-43
Hazardous Substances Data Bank. GLUCOSE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of type IV collagen alpha chains of glomerular epithelial cells in diabetic conditions.
  • Although type IV collagen is the main component of thickened GBM in diabetic nephropathy, cellular metabolism of each alpha chains of type IV collagen has not been well studied.
  • To investigate the regulation of alpha(IV) chains in diabetic conditions, we examined whether glucose and advanced glycosylation endproduct (AGE) regulate the metabolism of each alpha(IV) chains in the diabetic tissue and glomerular epithelial cells (GEpC).
  • In vitro, mainly high glucose and partly AGE usually increased total collagen protein of GEpC by [(3)H]-proline incorporation assay and each alpha(IV) chain proteins including alpha1(IV), alpha3(IV), and alpha5(IV) in time-dependent and subchain-specific manners.
  • However, the changes of each alpha(IV) chains mRNA expression was not well correlated to the those of each chain proteins.
  • The present findings suggest that the metabolism of individual alpha(IV) chains of GBM is differentially regulated in diabetic conditions and those changes might be induced not only by transcriptional level but also by post-translational modifications.
  • [MeSH-major] Collagen Type IV / metabolism. Diabetic Nephropathies / metabolism. Epithelial Cells / metabolism. Podocytes / metabolism

  • MedlinePlus Health Information. consumer health - Diabetic Kidney Problems.
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  • [Cites] Hypertension. 2001 Apr;37(4):1053-9 [11304502.001]
  • [Cites] J Biol Chem. 2000 Sep 29;275(39):30716-24 [10896941.001]
  • [Cites] N Engl J Med. 2003 Jun 19;348(25):2543-56 [12815141.001]
  • [Cites] J Am Soc Nephrol. 2003 Dec;14(12):3178-87 [14638916.001]
  • [Cites] Nephrol Dial Transplant. 2004 Jun;19(6):1437-40 [14993494.001]
  • [Cites] Pediatr Nephrol. 2004 Nov;19(11):1219-24 [15449170.001]
  • [Cites] Kidney Int. 1978 Jul;14(1):21-30 [682422.001]
  • [Cites] Eur J Biochem. 1981 Nov;120(2):203-11 [6274634.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Feb;87(4):1606-10 [1689491.001]
  • [Cites] Am J Pathol. 1991 Feb;138(2):413-20 [1992766.001]
  • [Cites] Diabetes. 1992 Dec;41(12):1520-7 [1280237.001]
  • [Cites] Am J Kidney Dis. 1993 Nov;22(5):736-44 [8238022.001]
  • [Cites] J Clin Invest. 1994 Feb;93(2):536-42 [8113392.001]
  • [Cites] Kidney Int. 1994 Feb;45(2):425-33 [8164429.001]
  • [Cites] J Cell Biol. 1994 Nov;127(3):879-91 [7962065.001]
  • [Cites] Nephron. 1995;70(1):42-8 [7617116.001]
  • [Cites] Diabetes. 1995 Oct;44(10):1139-46 [7556948.001]
  • [Cites] Semin Nephrol. 1997 Mar;17(2):80-92 [9148380.001]
  • [Cites] Curr Opin Nephrol Hypertens. 1998 Jan;7(1):13-9 [9442357.001]
  • [Cites] J Mol Med (Berl). 1998 Mar;76(3-4):253-65 [9535559.001]
  • [Cites] Lancet. 1998 Jul 18;352(9123):213-9 [9683226.001]
  • [Cites] Lancet. 1998 Sep 12;352(9131):837-53 [9742976.001]
  • [Cites] Kidney Int. 1998 Oct;54(4):1107-16 [9767526.001]
  • [Cites] Nephron. 1999 Sep;83(1):53-8 [10461036.001]
  • [Cites] Diabetes. 2005 Jun;54(6):1626-34 [15919782.001]
  • [Cites] Nephrol Dial Transplant. 2005 Jul;20(7):1320-8 [15840669.001]
  • [Cites] Cell Physiol Biochem. 2006;17(1-2):57-68 [16543722.001]
  • [Cites] Am J Physiol Renal Physiol. 2007 Feb;292(2):F789-95 [17018845.001]
  • [Cites] Kidney Int. 1999 Dec;56(6):2016-24 [10594777.001]
  • [Cites] Methods Cell Biol. 2002;69:111-44 [12070988.001]
  • (PMID = 19794980.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Collagen Type IV; 0 / Glycosylation End Products, Advanced; 0 / RNA, Messenger; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2752765
  • [Keywords] NOTNLM ; Collagen Type IV / Diabetic Nephropathies / Glucose / Glycosylation End Products, Advanced / Podocytes
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66. Nold-Petry CA, Nold MF, Nielsen JW, Bustamante A, Zepp JA, Storm KA, Hong JW, Kim SH, Dinarello CA: Increased cytokine production in interleukin-18 receptor alpha-deficient cells is associated with dysregulation of suppressors of cytokine signaling. J Biol Chem; 2009 Sep 18;284(38):25900-11
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] Increased cytokine production in interleukin-18 receptor alpha-deficient cells is associated with dysregulation of suppressors of cytokine signaling.
  • Unexpectedly, we observed a paradoxical 10-fold increase in IL-1beta-induced IL-6 production in MEF cells from mice deficient in the IL-18R alpha-chain (IL-18Ralpha) compared with wild type MEF.
  • Likewise, coincubation with a specific IL-18Ralpha-blocking antibody augmented IL-1beta-induced cytokines in wild type and IL-18 ko MEF.
  • Stable lines of IL-18Ralpha-depleted human A549 cells were generated using shRNA, resulting in an increase of IL-1beta-induced IL-1alpha, IL-6, and IL-8 compared to scrambled small hairpin RNA.
  • In addition, we silenced IL-18Ralpha with small interfering RNA in primary human blood cells and observed up to 4-fold increases in the secretion of lipopolysaccharide- and IL-12/IL-18-induced IL-1beta, IL-6, interferon-gamma, and CD40L.

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  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • [Cites] J Immunol. 1999 May 1;162(9):5041-4 [10227969.001]
  • [Cites] Immunity. 1999 Jan;10(1):127-36 [10023777.001]
  • [Cites] Arthritis Rheum. 2005 Mar;52(3):984-6 [15751069.001]
  • [Cites] J Immunol. 2005 Jul 1;175(1):276-85 [15972659.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3483-9 [16020503.001]
  • [Cites] Nat Immunol. 2006 Feb;7(2):148-55 [16415872.001]
  • [Cites] Nat Med. 2006 Jun;12(6):650-6 [16732281.001]
  • [Cites] Mol Endocrinol. 2006 Jul;20(7):1587-96 [16543409.001]
  • [Cites] Nat Immunol. 2006 Sep;7(9):946-53 [16906165.001]
  • [Cites] Mol Med. 2006 Jul-Aug;12(7-8):185-95 [17088951.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 7;103(45):16852-7 [17075045.001]
  • [Cites] J Immunol. 2007 Feb 1;178(3):1948-59 [17237446.001]
  • [Cites] Eur Cytokine Netw. 2006 Dec;17(4):224-52 [17353157.001]
  • [Cites] Nat Rev Immunol. 2007 Jun;7(6):454-65 [17525754.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jun 26;104(26):11097-102 [17578927.001]
  • [Cites] J Biochem Mol Biol. 2007 Jul 31;40(4):562-70 [17669273.001]
  • [Cites] J Immunol. 2008 Feb 15;180(4):2322-8 [18250441.001]
  • [Cites] Nat Rev Microbiol. 2008 Apr;6(4):266-75 [18311165.001]
  • [Cites] Immunity. 2008 Apr;28(4):477-87 [18400190.001]
  • [Cites] J Immunol. 2008 Jul 1;181(1):557-65 [18566422.001]
  • [Cites] Nat Immunol. 2008 Sep;9(9):1028-36 [18690222.001]
  • [Cites] Semin Cell Dev Biol. 2008 Aug;19(4):414-22 [18708154.001]
  • [Cites] J Clin Invest. 1999 Nov;104(10):1393-401 [10562301.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):734-9 [10639148.001]
  • [Cites] J Immunol. 2000 Nov 1;165(9):4950-6 [11046021.001]
  • [Cites] Arthritis Res. 2000;2(5):361-7 [11094449.001]
  • [Cites] Eur J Immunol. 2001 Feb;31(2):369-75 [11180100.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Feb 27;98(5):2871-6 [11226333.001]
  • [Cites] Annu Rev Immunol. 2001;19:423-74 [11244043.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2001 Oct;281(4):R1264-73 [11557635.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Oct 9;98(21):12191-6 [11593036.001]
  • [Cites] J Infect Dis. 2002 Apr 1;185(7):963-70 [11920321.001]
  • [Cites] Gut. 2002 Jun;50(6):812-20 [12010883.001]
  • [Cites] J Interferon Cytokine Res. 2002 May;22(5):593-601 [12060498.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2002 Aug;283(2):H650-7 [12124212.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Aug 20;99(17):11340-5 [12151598.001]
  • [Cites] Immunity. 2002 Nov;17(5):583-91 [12433365.001]
  • [Cites] Cytokine. 2003 Jan 21;21(2):65-73 [12670445.001]
  • [Cites] J Lab Clin Med. 2003 Jun;141(6):365-71 [12819633.001]
  • [Cites] Scand J Gastroenterol. 2003 Aug;38(8):837-44 [12940437.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14181-6 [14615579.001]
  • [Cites] Mol Cell. 2003 Dec;12(6):1413-26 [14690596.001]
  • [Cites] Biochim Biophys Acta. 2004 Mar 22;1636(2-3):108-18 [15164758.001]
  • [Cites] J Immunol. 2004 Oct 15;173(8):5312-8 [15470078.001]
  • [Cites] Brain Res. 1991 Oct 25;562(2):199-206 [1773338.001]
  • [Cites] Kidney Int. 1995 Mar;47(3):837-44 [7752582.001]
  • [Cites] Kidney Int. 1995 Mar;47(3):845-54 [7752583.001]
  • [Cites] Science. 1997 Jan 10;275(5297):206-9 [8999548.001]
  • [Cites] Nature. 1997 Apr 10;386(6625):619-23 [9121587.001]
  • [Cites] Blood. 1998 Mar 15;91(6):2118-25 [9490698.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Mar 25;328(4):953-61 [15707970.001]
  • (PMID = 19592492.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI015614; United States / NIAID NIH HHS / AI / R56 AI015614; United States / NIAID NIH HHS / AI / AI 15614; United States / NCI NIH HHS / CA / CA-04 6934
  • [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 / Cytokines; 0 / IL18R1 protein, human; 0 / Il18r1 protein, mouse; 0 / Interleukin-18; 0 / Interleukin-18 Receptor alpha Subunit; 0 / SOCS1 protein, human; 0 / SOCS3 protein, human; 0 / Socs1 protein, mouse; 0 / Socs3 protein, mouse; 0 / Suppressor of Cytokine Signaling Proteins; EC 2.7.- / Protein Kinases
  • [Other-IDs] NLM/ PMC2757991
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67. Lowanitchapat A, Payungporn S, Sereemaspun A, Ekpo P, Phulsuksombati D, Poovorawan Y, Chirathaworn C: Expression of TNF-alpha, TGF-beta, IP-10 and IL-10 mRNA in kidneys of hamsters infected with pathogenic Leptospira. Comp Immunol Microbiol Infect Dis; 2010 Sep;33(5):423-34

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of TNF-alpha, TGF-beta, IP-10 and IL-10 mRNA in kidneys of hamsters infected with pathogenic Leptospira.
  • Although several components of this organism have been identified, the molecular mechanisms underlying pathogenesis of this infectious disease are still poorly understood.
  • Real-time PCR was performed to demonstrate expression of TNF-alpha, TGF-beta, IP-10 and IL-10 mRNA in kidneys.
  • TNF-alpha, TGF-beta and IP-10 expression could be demonstrated since day 3 post-infection whereas IL-10 expression was detected later on day 5.
  • Leptospira infection resulted in not only expression of a proinflammatory cytokine, TNF-alpha, but also a T cell chemokine, IP-10.
  • [MeSH-major] Chemokine CXCL10 / genetics. Interleukin-10 / genetics. Leptospira interrogans / pathogenicity. Leptospirosis / genetics. Leptospirosis / immunology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Transforming Growth Factor beta / genetics. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Animals. Base Sequence. Cricetinae. DNA Primers / genetics. Disease Models, Animal. Gene Expression. Kidney / immunology. Mesocricetus. RNA, Ribosomal, 16S / genetics. Reverse Transcriptase Polymerase Chain Reaction. Zoonoses / microbiology

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19559480.001).
  • [ISSN] 1878-1667
  • [Journal-full-title] Comparative immunology, microbiology and infectious diseases
  • [ISO-abbreviation] Comp. Immunol. Microbiol. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokine CXCL10; 0 / DNA Primers; 0 / RNA, Messenger; 0 / RNA, Ribosomal, 16S; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
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68. Calafat M, Larocca L, Roca V, Hauk V, Pregi N, Nesse A, Pérez Leirós C: Vasoactive intestinal peptide inhibits TNF-alpha-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands. Arthritis Res Ther; 2009;11(2):R53
MedlinePlus Health Information. consumer health - Sjogren's Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vasoactive intestinal peptide inhibits TNF-alpha-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands.
  • Vasoactive intestinal peptide (VIP) has anti-inflammatory effects in various models of chronic inflammation.
  • Our goal was to analyse the effect of TNF-alpha on apoptotic mediators in isolated acinar cells from NOD submandibular gland and their modulation by VIP.
  • Apoptotic mediators and TNF-alpha receptor expression were assessed by immunoblotting and RT-PCR, caspase 3 activity was assessed by optical density at 405 nm with Ac-DEVD-pNA as a substrate and chromatin condensation by Hoechst stain.
  • They were evaluated in resting conditions and after a 3.5 or 6 hours of culture with TNF-alpha.
  • VIP effects in acinar cells were assessed at 100 nM in TNF-alpha-treated cultures and VIP receptor functional assays by radio immunoassay (cAMP) or enzymatic detection (amylase).
  • RESULTS: NOD acinar cells at 16 weeks present an increased expression of TNF-alpha receptor1 together with increased Bax, tumour protein 53-induced nuclear protein1alpha (TP53INP1alpha), caspase 3 activity and chromatin condensation.
  • Acini from NOD mice were more sensitive to TNF-alpha-induced increases of apoptotic mediators than control cells.
  • VIP inhibited TNF-alpha-induced apoptotic events through functional VPAC1 receptors coupled to the protein kinase A (PKA) signalling pathway.
  • CONCLUSIONS: Our results indicate that acinar cells isolated from submandibular glands of NOD mice with salivary dysfunction are more sensitive to apoptosis induced by TNF-alpha which could be prevented by VIP through a PKA-mediated pathway.
  • [MeSH-major] Apoptosis / physiology. Sjogren's Syndrome / metabolism. Submandibular Gland / metabolism. Tumor Necrosis Factor-alpha / metabolism. Vasoactive Intestinal Peptide / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cyclic AMP-Dependent Protein Kinases / metabolism. Disease Models, Animal. Female. Mice. Mice, Inbred BALB C. Mice, Inbred NOD. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / physiology

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  • [Cites] Ann N Y Acad Sci. 2006 Jul;1070:525-30 [16888219.001]
  • [Cites] Biochim Biophys Acta. 2006 Feb;1763(2):238-46 [16500719.001]
  • [Cites] Nat Clin Pract Rheumatol. 2006 May;2(5):252-61 [16932698.001]
  • [Cites] Rheumatology (Oxford). 2006 Sep;45(9):1077-86 [16522680.001]
  • [Cites] Lab Invest. 2006 Dec;86(12):1243-60 [17075579.001]
  • [Cites] Reproduction. 2006 Dec;132(6):931-8 [17127753.001]
  • [Cites] Nat Rev Immunol. 2007 Jan;7(1):52-63 [17186031.001]
  • [Cites] Int Immunopharmacol. 2007 Oct;7(10):1343-9 [17673149.001]
  • [Cites] Peptides. 2007 Sep;28(9):1825-32 [17706836.001]
  • [Cites] Arthritis Rheum. 2007 Nov;56(11):3588-600 [17968930.001]
  • [Cites] Neuroimmunomodulation. 2007;14(3-4):134-8 [18073504.001]
  • [Cites] Neuroimmunomodulation. 2007;14(3-4):175-81 [18073511.001]
  • [Cites] Arthritis Res Ther. 2008;10(1):R22 [18289371.001]
  • [Cites] Arthritis Res Ther. 2008;10(6):R137 [19032782.001]
  • [Cites] Baillieres Best Pract Res Clin Rheumatol. 2000 Mar;14(1):73-95 [10882215.001]
  • [Cites] J Immunol. 2001 Jan 15;166(2):1028-40 [11145682.001]
  • [Cites] J Autoimmun. 2001 Sep;17(2):141-53 [11591123.001]
  • [Cites] Eur J Pharmacol. 2002 Mar 29;439(1-3):27-33 [11937089.001]
  • [Cites] Clin Immunol. 2002 May;103(2):111-24 [12027416.001]
  • [Cites] Arch Oral Biol. 2002 Jun;47(6):443-8 [12102760.001]
  • [Cites] J Biol Chem. 2003 Sep 19;278(38):36676-87 [12867423.001]
  • [Cites] J Biol Chem. 2003 Sep 26;278(39):37722-9 [12851404.001]
  • [Cites] Endocrinology. 2004 Jan;145(1):418-25 [14500572.001]
  • [Cites] Bull Rheum Dis. 1979-1980;30(9):1046-52 [398729.001]
  • [Cites] Semin Arthritis Rheum. 1984 Nov;14(2):77-105 [6399627.001]
  • [Cites] In Vitro Cell Dev Biol. 1988 Apr;24(4):266-73 [3284875.001]
  • [Cites] Proc Finn Dent Soc. 1989;85(4-5):323-31; discussion 361-3 [2699762.001]
  • [Cites] Blood. 1996 Jun 15;87(12):5152-61 [8652828.001]
  • [Cites] Arthritis Rheum. 1997 Jan;40(1):87-97 [9008604.001]
  • [Cites] Lancet. 1997 Jun 21;349(9068):1814-5 [9269222.001]
  • [Cites] J Clin Invest. 1997 Oct 1;100(7):1853-62 [9312187.001]
  • [Cites] Clin Immunol Immunopathol. 1998 Aug;88(2):133-41 [9714690.001]
  • [Cites] Clin Exp Rheumatol. 1998 Nov-Dec;16(6):675-81 [9844759.001]
  • [Cites] Int Immunopharmacol. 2004 Dec 20;4(14):1837-44 [15531299.001]
  • [Cites] Br J Pharmacol. 2004 Dec;143(8):1058-65 [15533891.001]
  • [Cites] Immunology. 2005 May;115(1):1-20 [15819693.001]
  • [Cites] Clin Exp Immunol. 2005 Dec;142(3):411-8 [16297151.001]
  • [Cites] Oncogene. 2005 Dec 8;24(55):8093-104 [16044147.001]
  • [Cites] Ann Rheum Dis. 2006 Feb;65(2):195-200 [15975969.001]
  • [Cites] Arthritis Rheum. 2006 Jul;54(7):2300-5 [16802370.001]
  • (PMID = 19356238.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 37221-79-7 / Vasoactive Intestinal Peptide; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Other-IDs] NLM/ PMC2688204
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69. Zer C, Sachs G, Shin JM: Identification of genomic targets downstream of p38 mitogen-activated protein kinase pathway mediating tumor necrosis factor-alpha signaling. Physiol Genomics; 2007 Oct 22;31(2):343-51
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] Identification of genomic targets downstream of p38 mitogen-activated protein kinase pathway mediating tumor necrosis factor-alpha signaling.
  • Inhibition of p38 MAPK suppresses the expression of proinflammatory cytokines such as TNF-alpha and IL-1 beta in macrophages and fibroblast-like synoviocytes (FLS).
  • Four independent sets of mRNA modulated by TNF-alpha and vehicle were used to measure the change of gene expression due to TNF-alpha, and three experiments were done to ascertain the effect of SB-203580, a p38 MAPK inhibitor, on TNF-alpha-induced genes.
  • Microarray data were validated by RT-quantitative polymerase chain reaction.
  • One hundred forty-one significantly expressed genes were more than twofold upregulated by TNF-alpha.
  • Approximately one-third of the TNF-alpha-induced genes in FLS are regulated by the p38 MAPK signal pathway, showing that p38 MAPK is a possible target for suppressing proinflammatory gene expressions in rheumatoid arthritis.

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  • [Cites] J Autoimmun. 2000 Nov;15(3):301-13 [11040071.001]
  • [Cites] Arthritis Res Ther. 2006;8(4):R107 [16846531.001]
  • [Cites] Am J Pathol. 2000 Dec;157(6):2037-44 [11106576.001]
  • [Cites] Arthritis Rheum. 2000 Dec;43(12):2619-33 [11145019.001]
  • [Cites] Arthritis Res. 2001;3(1):72-6 [11178129.001]
  • [Cites] J Steroid Biochem Mol Biol. 2001 Jun;77(4-5):185-91 [11457656.001]
  • [Cites] Curr Opin Chem Biol. 2001 Aug;5(4):432-8 [11470607.001]
  • [Cites] J Biol Chem. 2002 Mar 22;277(12):9790-9 [11773051.001]
  • [Cites] Arthritis Rheum. 2002 Mar;46(3):824-36 [11920421.001]
  • [Cites] Nucleic Acids Res. 2002 May 1;30(9):e36 [11972351.001]
  • [Cites] J Med Chem. 2002 Oct 10;45(21):4695-705 [12361396.001]
  • [Cites] Cell Death Differ. 2003 Jan;10(1):45-65 [12655295.001]
  • [Cites] Infect Immun. 2003 May;71(5):2542-7 [12704126.001]
  • [Cites] Nat Rev Drug Discov. 2003 Jun;2(6):473-88 [12776222.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2807-16 [12855661.001]
  • [Cites] Arthritis Rheum. 2003 Aug;48(8):2155-62 [12905468.001]
  • [Cites] FEBS Lett. 2003 Sep 11;551(1-3):8-12 [12965196.001]
  • [Cites] Arthritis Rheum. 2004 Feb;50(2):420-31 [14872484.001]
  • [Cites] Mol Cell Proteomics. 2004 Aug;3(8):820-33 [15169874.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Nov 5;324(1):3-7 [15464974.001]
  • [Cites] Ann Rheum Dis. 2004 Nov;63(11):1453-9 [15479895.001]
  • [Cites] Rheumatology (Oxford). 2004 Nov;43(11):1346-52 [15292528.001]
  • [Cites] J Exp Med. 1985 Dec 1;162(6):2163-8 [2999289.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Jan;86(2):612-6 [2643119.001]
  • [Cites] J Immunol. 1990 May 1;144(9):3347-53 [2109776.001]
  • [Cites] J Immunol Methods. 1990 Oct 4;133(1):31-8 [2212689.001]
  • [Cites] Ann Rheum Dis. 1990 Sep;49(9):665-7 [1700672.001]
  • [Cites] Clin Rheumatol. 1991 Dec;10(4):374-6 [1802490.001]
  • [Cites] Br J Rheumatol. 1992 Nov;31(11):725-33 [1304740.001]
  • [Cites] Nature. 1994 Dec 22-29;372(6508):739-46 [7997261.001]
  • [Cites] FEBS Lett. 1995 May 8;364(2):229-33 [7750577.001]
  • [Cites] Semin Arthritis Rheum. 1996 Aug;26(1):435-46 [8870111.001]
  • [Cites] Am J Pathol. 1996 Nov;149(5):1607-15 [8909250.001]
  • [Cites] J Cell Biol. 1997 Feb 24;136(4):935-44 [9049257.001]
  • [Cites] EMBO J. 1997 Jun 16;16(12):3563-71 [9218798.001]
  • [Cites] J Clin Invest. 1998 Mar 1;101(5):1163-74 [9486988.001]
  • [Cites] J Biol Chem. 1998 Jun 19;273(25):15605-10 [9624152.001]
  • [Cites] J Pharmacol Exp Ther. 1999 Oct;291(1):124-30 [10490895.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Oct 5;263(3):825-31 [10512765.001]
  • [Cites] J Biol Chem. 2004 Dec 17;279(51):53725-35 [15471861.001]
  • [Cites] Scand J Immunol. 2005 Jan;61(1):18-28 [15644119.001]
  • [Cites] Inflamm Res. 2005 Jan;54(1):10-6 [15723199.001]
  • [Cites] J Biol Chem. 2005 Apr 29;280(17):17435-48 [15722553.001]
  • [Cites] BMC Bioinformatics. 2005;6:86 [15813968.001]
  • [Cites] Int J Cancer. 2005 Aug 20;116(2):243-52 [15812828.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Sep 9;334(4):973-8 [16038875.001]
  • [Cites] Clin Exp Rheumatol. 2005 Sep-Oct;23(5):644-50 [16173240.001]
  • [Cites] J Rheumatol. 2005 Dec;32(12):2291-8 [16331752.001]
  • [Cites] Curr Med Chem. 2005;12(25):2979-94 [16378500.001]
  • [Cites] Nat Rev Immunol. 2006 Jul;6(7):532-40 [16799472.001]
  • [Cites] Autoimmunity. 2006 Jun;39(4):307-13 [16891219.001]
  • [Cites] J Rheumatol. 2006 Sep;33(9):1754-9 [16960937.001]
  • [Cites] Rheumatol Int. 2006 Sep;26(11):972-8 [16532349.001]
  • [Cites] Arthritis Rheum. 2006 Sep;54(9):2745-56 [16947383.001]
  • [Cites] Arthritis Rheum. 2006 Nov;54(11):3399-407 [17075823.001]
  • [Cites] Arthritis Rheum. 2000 Nov;43(11):2501-12 [11083274.001]
  • (PMID = 17652167.001).
  • [ISSN] 1531-2267
  • [Journal-full-title] Physiological genomics
  • [ISO-abbreviation] Physiol. Genomics
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK046917-09; United States / NIDDK NIH HHS / DK / DK-46917; United States / NIDDK NIH HHS / DK / R01 DK058333-09; United States / NIDDK NIH HHS / DK / R01 DK046917; United States / NIDDK NIH HHS / DK / DK058333-09; United States / NIDDK NIH HHS / DK / DK-41301; United States / NIDDK NIH HHS / DK / DK046917-09; United States / NIDDK NIH HHS / DK / P30 DK041301; United States / NIDDK NIH HHS / DK / DK-58333; United States / NIDDK NIH HHS / DK / R56 DK058333; United States / NIDDK NIH HHS / DK / DK-53462; United States / NIDDK NIH HHS / DK / R01 DK058333
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CXCL2; 0 / Chemokines, CXC; 0 / Cxcl2 protein, rat; 0 / Gm1960 protein, rat; 0 / Imidazoles; 0 / Pyridines; 0 / RNA, Messenger; 0 / SB 203580; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS187160; NLM/ PMC2880477
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70. Boyer JF, Balard P, Authier H, Faucon B, Bernad J, Mazières B, Davignon JL, Cantagrel A, Pipy B, Constantin A: Tumor necrosis factor alpha and adalimumab differentially regulate CD36 expression in human monocytes. Arthritis Res Ther; 2007;9(2):R22

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor necrosis factor alpha and adalimumab differentially regulate CD36 expression in human monocytes.
  • In chronic inflammatory diseases, such as rheumatoid arthritis, inflammation acts as an independent cardiovascular risk factor and the use of anti-inflammatory drugs, such as anti-tumor necrosis factor alpha (anti-TNFalpha), may decrease this risk.
  • Further studies are needed to investigate the clinical implications of these results in accelerated atherosclerosis observed in rheumatoid arthritis.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Antibodies, Monoclonal / pharmacology. Antigens, CD36 / drug effects. Monocytes / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Adalimumab. Antibodies, Monoclonal, Humanized. Arthritis, Rheumatoid / complications. Arthritis, Rheumatoid / metabolism. Arthritis, Rheumatoid / physiopathology. Atherosclerosis / etiology. Atherosclerosis / metabolism. Atherosclerosis / physiopathology. Cells, Cultured. Electrophoretic Mobility Shift Assay. Flow Cytometry. Gene Expression / drug effects. Humans. Immunoglobulin Fab Fragments / pharmacology. PPAR gamma / metabolism. RNA, Messenger / drug effects. Reactive Oxygen Species / analysis. Reactive Oxygen Species / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] J Leukoc Biol. 1999 Dec;66(6):909-14 [10614771.001]
  • [Cites] Blood. 1996 Mar 1;87(5):2020-8 [8634453.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2000 Apr;278(4):H1042-8 [10749696.001]
  • [Cites] J Clin Invest. 2000 Apr;105(8):1049-56 [10772649.001]
  • [Cites] Circulation. 2000 Jul 4;102(1):82-7 [10880419.001]
  • [Cites] Nature. 2000 Sep 14;407(6801):233-41 [11001066.001]
  • [Cites] Science. 2001 Jan 19;291(5503):484-6 [11161202.001]
  • [Cites] J Lipid Res. 2001 Apr;42(4):521-7 [11290823.001]
  • [Cites] J Biol Chem. 2001 Jun 22;276(25):23077-83 [11304537.001]
  • [Cites] J Clin Invest. 2001 Sep;108(6):785-91 [11560944.001]
  • [Cites] Blood. 2001 Dec 1;98(12):3421-8 [11719383.001]
  • [Cites] Atherosclerosis. 2002 Apr;161(2):307-16 [11888513.001]
  • [Cites] Lancet. 2002 Apr 6;359(9313):1173-7 [11955534.001]
  • [Cites] Circulation. 2002 Oct 22;106(17):2184-7 [12390945.001]
  • [Cites] Immunol Res. 2002;26(1-3):95-105 [12403349.001]
  • [Cites] J Biol Chem. 2002 Dec 20;277(51):49982-8 [12376530.001]
  • [Cites] J Biol Chem. 1997 May 16;272(20):12938-44 [9148899.001]
  • [Cites] Nature. 1998 Jan 1;391(6662):82-6 [9422509.001]
  • [Cites] Circulation. 1998 Jan 27;97(3):242-4 [9462524.001]
  • [Cites] Am J Physiol. 1998 Feb;274(2 Pt 1):E210-7 [9486149.001]
  • [Cites] EMBO J. 1999 Apr 15;18(8):2119-26 [10205166.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 1999 May;19(5):1333-9 [10323787.001]
  • [Cites] Nature. 1999 Jul 22;400(6742):378-82 [10432118.001]
  • [Cites] Trends Mol Med. 2004 Nov;10(11):549-57 [15519281.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2004 Nov;24(11):2137-42 [15345516.001]
  • [Cites] Ann Rheum Dis. 2005 Feb;64(2):303-5 [15231512.001]
  • [Cites] Gastroenterology. 2005 Feb;128(2):376-92 [15685549.001]
  • [Cites] Arthritis Rheum. 2005 Mar;52(3):722-32 [15751097.001]
  • [Cites] Cardiovasc Res. 2005 Apr 1;66(1):141-9 [15769457.001]
  • [Cites] Curr Opin Rheumatol. 2005 May;17(3):234-41 [15838230.001]
  • [Cites] Semin Arthritis Rheum. 2005 Apr;34(5 Suppl1):12-8 [15852249.001]
  • [Cites] J Rheumatol. 2005 Jul;32(7):1213-8 [15996054.001]
  • [Cites] Nat Cell Biol. 2003 Mar;5(3):224-30 [12598905.001]
  • [Cites] Trends Cardiovasc Med. 2003 May;13(4):136-41 [12732446.001]
  • [Cites] Heart. 2003 Sep;89(9):993-7 [12923007.001]
  • [Cites] Biochem Pharmacol. 2004 Jan 15;67(2):303-13 [14698043.001]
  • [Cites] Circ Res. 2004 Mar 19;94(5):609-16 [14752028.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 May;286(5):G722-9 [14656714.001]
  • [Cites] J Clin Invest. 2005 Aug;115(8):2192-201 [16075060.001]
  • [Cites] Semin Arthritis Rheum. 2005 Aug;35(1):8-17 [16084219.001]
  • [Cites] Toxicon. 2005 Dec 15;46(8):876-82 [16260020.001]
  • [Cites] Cardiovasc Res. 2006 Feb 1;69(2):527-35 [16336952.001]
  • [Cites] Circulation. 2004 Apr 13;109(14):1718-23 [15037536.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2004 Jun;24(6):1006-14 [15087308.001]
  • [Cites] Lancet. 2004 Jun 19;363(9426):2015-21 [15207950.001]
  • [Cites] Cytokine Growth Factor Rev. 2004 Oct;15(5):353-66 [15450251.001]
  • [Cites] J Biol Chem. 1989 Aug 25;264(24):14112-20 [