[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 9 of about 9
1. Shearn CT, Backos DS, Orlicky DJ, Smathers-McCullough RL, Petersen DR: Identification of 5' AMP-activated kinase as a target of reactive aldehydes during chronic ingestion of high concentrations of ethanol. J Biol Chem; 2014 May 30;289(22):15449-62
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of 5' AMP-activated kinase as a target of reactive aldehydes during chronic ingestion of high concentrations of ethanol.
  • In an in vitro cellular model, we identified AMPK as a direct target of 4-HNE adduction resulting in inhibition of both H2O2 and 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR)-induced downstream signaling.
  • The observed inhibition of AMPK by 4-HNE provides a novel mechanism for altered β-oxidation in ALD, and these data demonstrate for the first time that AMPK is subject to regulation by reactive aldehydes in vivo.

  • Hazardous Substances Data Bank. ETHANOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
  • [Cites] Biochem Biophys Res Commun. 2001 Sep 14;287(1):92-7 [11549258.001]
  • [Cites] PLoS One. 2012;7(6):e38459 [22701647.001]
  • [Cites] J Comput Chem. 2002 Nov 15;23(14):1297-304 [12214312.001]
  • [Cites] Cell Death Differ. 2003 Jul;10(7):772-81 [12815460.001]
  • [Cites] Alcohol Clin Exp Res. 2003 Jun;27(6):1015-22 [12824824.001]
  • [Cites] J Forensic Sci. 2003 Jul;48(4):874-9 [12877310.001]
  • [Cites] Mol Aspects Med. 2003 Aug-Oct;24(4-5):149-59 [12892992.001]
  • [Cites] Arch Biochem Biophys. 1978 Aug;189(2):364-71 [708057.001]
  • [Cites] Anal Biochem. 1980 Jul 15;106(1):55-62 [7416469.001]
  • [Cites] Biochim Biophys Acta. 1982 May 13;711(2):345-56 [7093302.001]
  • [Cites] Biochim Biophys Acta. 1982 Sep 14;712(3):628-38 [7126629.001]
  • [Cites] Biochim Biophys Acta. 1984 Feb 9;792(2):172-81 [6320898.001]
  • [Cites] Int J Biochem. 1987;19(9):879-84 [2961636.001]
  • [Cites] Clin Biochem. 1989 Feb;22(1):41-9 [2650922.001]
  • [Cites] Free Radic Biol Med. 1991;11(1):81-128 [1937131.001]
  • [Cites] J Pharmacol Exp Ther. 1993 Feb;264(2):944-50 [8437134.001]
  • [Cites] Free Radic Biol Med. 2012 Jul 1;53(1):1-11 [22580126.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2013 Jan 1;304(1):G38-47 [23139221.001]
  • [Cites] J Lipid Res. 2013 May;54(5):1335-45 [23359610.001]
  • [Cites] J Nutr Biochem. 2013 Aug;24(8):1436-45 [23465594.001]
  • [Cites] J Biol Chem. 2013 Aug 30;288(35):25007-24 [23836899.001]
  • [Cites] Methods Enzymol. 1994;233:585-94 [8015491.001]
  • [Cites] Alcohol Alcohol. 1992 Nov;27(6):641-7 [1292437.001]
  • [Cites] Free Radic Biol Med. 2013 Dec;65:680-92 [23872024.001]
  • [Cites] Hepatology. 1997 Jul;26(1):135-42 [9214462.001]
  • [Cites] J Clin Pathol. 1997 May;50(5):401-6 [9215123.001]
  • [Cites] Arch Biochem Biophys. 1998 Feb 15;350(2):193-200 [9473292.001]
  • [Cites] Gastroenterology. 2004 Dec;127(6):1798-808 [15578517.001]
  • [Cites] Protein Expr Purif. 2005 Sep;43(1):44-56 [16084396.001]
  • [Cites] Hepatology. 2005 Sep;42(3):568-77 [16108051.001]
  • [Cites] J Biol Chem. 2006 Feb 3;281(5):2598-604 [16311241.001]
  • [Cites] Chem Res Toxicol. 2007 Aug;20(8):1111-9 [17630713.001]
  • [Cites] Biochimie. 2008 Mar;90(3):460-6 [17997005.001]
  • [Cites] Int J Mol Med. 2008 Apr;21(4):507-11 [18360697.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2008 Jul;295(1):E10-6 [18349117.001]
  • [Cites] Free Radic Biol Med. 2008 Dec 1;45(11):1551-8 [18852041.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2008 Dec;295(6):G1173-81 [18832448.001]
  • [Cites] Lab Invest. 2009 Mar;89(3):315-26 [19153555.001]
  • [Cites] Mol Cell Proteomics. 2009 Apr;8(4):670-80 [19054759.001]
  • [Cites] J Comput Chem. 2009 Jul 30;30(10):1545-614 [19444816.001]
  • [Cites] J Pharmacol Exp Ther. 2009 Jul;330(1):79-88 [19386791.001]
  • [Cites] Biochem Biophys Res Commun. 1993 Feb 15;190(3):780-5 [8439329.001]
  • [Cites] Cell Cycle. 2009 Aug 15;8(16):2502-8 [19597332.001]
  • [Cites] J Biol Chem. 2009 Oct 9;284(41):27816-26 [19648649.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2010 Mar;298(3):G364-74 [20007851.001]
  • [Cites] J Clin Invest. 2010 Jul;120(7):2267-70 [20577046.001]
  • [Cites] Cell Signal. 2010 Oct;22(10):1469-76 [20639120.001]
  • [Cites] Biochemistry. 2010 Jul 27;49(29):6263-75 [20565132.001]
  • [Cites] Hepatology. 2010 Sep;52(3):934-44 [20607689.001]
  • [Cites] J Biol Chem. 2010 Oct 22;285(43):33154-64 [20729205.001]
  • [Cites] Proc Natl Acad Sci U S A. 2010 Nov 9;107(45):19237-41 [20974912.001]
  • [Cites] Exp Eye Res. 2010 Dec;91(6):818-24 [21029733.001]
  • [Cites] Nature. 2011 Apr 14;472(7342):230-3 [21399626.001]
  • [Cites] Biochemistry. 2011 May 17;50(19):3984-96 [21438592.001]
  • [Cites] Mol Pharmacol. 2011 Jun;79(6):941-52 [21415306.001]
  • [Cites] Hepatology. 2011 Jun;53(6):1895-905 [21391224.001]
  • [Cites] J Hepatol. 2011 Sep;55(3):673-82 [21256905.001]
  • [Cites] Alcohol Clin Exp Res. 2011 Dec;35(12):2139-51 [21790669.001]
  • [Cites] Hepatology. 2012 May;55(5):1596-609 [22213272.001]
  • [Cites] Chem Res Toxicol. 2012 May 21;25(5):1012-21 [22502949.001]
  • [Cites] In Vitr Mol Toxicol. 2001 Fall;14(3):177-90 [11846991.001]
  • (PMID = 24722988.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / UL1 RR025780; United States / NIAAA NIH HHS / AA / R56 AA009300; United States / NIAAA NIH HHS / AA / R37AA009300-17; United States / NCI NIH HHS / CA / P30 CA046934; United States / NIAAA NIH HHS / AA / F32 AA018613; United States / NIAAA NIH HHS / AA / R37 AA009300; United States / NIAAA NIH HHS / AA / F32 AA018613-03; United States / NCATS NIH HHS / TR / UL1 TR001082
  • [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 / Aldehydes; 0 / Central Nervous System Depressants; 0 / Cysteine Proteinase Inhibitors; 29343-52-0 / 4-hydroxy-2-nonenal; 3K9958V90M / Ethanol; EC 2.7.11.1 / AMP-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC4140901
  • [Keywords] NOTNLM ; AMP-activated Kinase (AMPK) / Alcohol / Lipid Peroxidation / Liver / Oxidative Stress
  •  go-up   go-down


2. Sojka DK, Fowell DJ: Regulatory T cells inhibit acute IFN-γ synthesis without blocking T-helper cell type 1 (Th1) differentiation via a compartmentalized requirement for IL-10. Proc Natl Acad Sci U S A; 2011 Nov 08;108(45):18336-41
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We developed in vitro and in vivo models that enabled the direct test of Treg regulation of T-helper cell type 1 (Th1) differentiation.
  • Interestingly, Tregs used different regulatory mechanisms to regulate IFN-γ (IL-10-dependent or -independent) subject to the target T-cell stage of activation and its tissue location.
  • [MeSH-minor] Animals. Cell Compartmentation. Cell Lineage. Flow Cytometry. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Immunol. 2002 Jun;3(6):549-57 [12006974.001]
  • [Cites] Immunity. 2011 Apr 22;34(4):566-78 [21511185.001]
  • [Cites] J Immunol. 2003 Jul 15;171(2):971-8 [12847269.001]
  • [Cites] J Immunol. 2004 Sep 1;173(5):2942-51 [15322152.001]
  • [Cites] Science. 1989 Apr 21;244(4902):339-43 [2540528.001]
  • [Cites] J Immunol. 1993 Aug 1;151(3):1224-34 [7687627.001]
  • [Cites] J Exp Med. 1998 Jul 20;188(2):287-96 [9670041.001]
  • [Cites] Int Immunol. 1998 Dec;10(12):1969-80 [9885918.001]
  • [Cites] J Exp Med. 1999 Oct 4;190(7):995-1004 [10510089.001]
  • [Cites] J Immunol. 2004 Dec 15;173(12):7120-4 [15585831.001]
  • [Cites] J Immunol. 2005 May 1;174(9):5444-55 [15845457.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3097-104 [16014565.001]
  • [Cites] J Immunol. 2005 Dec 1;175(11):7135-42 [16301616.001]
  • [Cites] J Immunol. 2005 Dec 1;175(11):7274-80 [16301632.001]
  • [Cites] Immunity. 2006 Jul;25(1):129-41 [16860762.001]
  • [Cites] J Immunol. 2006 Nov 1;177(9):5852-60 [17056509.001]
  • [Cites] J Immunol. 2006 Nov 15;177(10):6780-6 [17082591.001]
  • [Cites] J Exp Med. 2007 Jun 11;204(6):1303-10 [17502663.001]
  • [Cites] J Exp Med. 2007 Jun 11;204(6):1335-47 [17548521.001]
  • [Cites] Nat Med. 2007 Jul;13(7):843-50 [17558415.001]
  • [Cites] Nature. 2007 Nov 22;450(7169):566-9 [18033300.001]
  • [Cites] Nat Immunol. 2008 Mar;9(3):239-44 [18285775.001]
  • [Cites] Immunity. 2008 Apr;28(4):546-58 [18387831.001]
  • [Cites] Immunity. 2008 Apr;28(4):468-76 [18400189.001]
  • [Cites] Immunology. 2008 May;124(1):13-22 [18346152.001]
  • [Cites] Immunity. 2008 Jun;28(6):763-73 [18549798.001]
  • [Cites] Immunity. 2009 Feb 20;30(2):277-88 [19200757.001]
  • [Cites] Nature. 2009 Mar 19;458(7236):351-6 [19182775.001]
  • [Cites] Annu Rev Immunol. 2009;27:551-89 [19302048.001]
  • [Cites] Immunity. 2009 Mar 20;30(3):458-69 [19303390.001]
  • [Cites] Nat Immunol. 2009 Jun;10(6):595-602 [19412181.001]
  • [Cites] Immunity. 2009 May;30(5):673-83 [19409816.001]
  • [Cites] Immunity. 2009 May;30(5):636-45 [19464986.001]
  • [Cites] Eur J Immunol. 2009 Jun;39(6):1544-51 [19462377.001]
  • [Cites] Immunity. 2009 Oct 16;31(4):654-64 [19818653.001]
  • [Cites] Science. 2009 Nov 13;326(5955):986-91 [19797626.001]
  • [Cites] Nat Immunol. 2010 Jan;11(1):7-13 [20016504.001]
  • [Cites] Annu Rev Immunol. 2010;28:445-89 [20192806.001]
  • [Cites] Int J Cancer. 2010 Aug 15;127(4):759-67 [20518016.001]
  • [Cites] Immunity. 2011 Apr 22;34(4):554-65 [21511184.001]
  • [Cites] J Immunol. 2003 Mar 15;170(6):2962-70 [12626548.001]
  • (PMID = 22025707.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI070826
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 130068-27-8 / Interleukin-10; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC3215041
  •  go-up   go-down


3. Kolling GL, Obata F, Gross LK, Obrig TG: Immunohistologic techniques for detecting the glycolipid Gb(3) in the mouse kidney and nervous system. Histochem Cell Biol; 2008 Jul;130(1):157-64
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistologic techniques for detecting the glycolipid Gb(3) in the mouse kidney and nervous system.
  • Thus, cell types that express Gb(3) in target tissues should be recognized.
  • In the mouse tissues studied, Gb(3) was associated with tubules in the kidney and neurons in the nervous system.
  • This finding was corroborated by glycolipid profiles from tissue subjected to dehydration; namely Gb(3) was subject to extraction by ethanol more than acetone during tissue dehydration.
  • The results of this study show that tissue preparation is crucial to the persistence and preservation of the glycolipid Gb(3) in mouse tissue.
  • [MeSH-major] Fluorescent Antibody Technique, Direct / methods. Frozen Sections / methods. Kidney Tubules / chemistry. Neurons / chemistry. Paraffin Embedding / methods. Trihexosylceramides / analysis
  • [MeSH-minor] Animals. Antibodies, Monoclonal / immunology. Hemolytic-Uremic Syndrome / metabolism. Hemolytic-Uremic Syndrome / microbiology. Male. Mice. Mice, Inbred C57BL. Shiga Toxins / metabolism. Shiga-Toxigenic Escherichia coli / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Brain Res. 1999 Apr 17;825(1-2):183-8 [10216186.001]
  • [Cites] Histochemie. 1973 Feb 6;34(2):143-56 [4568805.001]
  • [Cites] J Lipid Res. 1965 Jul;6:428-31 [14336214.001]
  • [Cites] J Clin Invest. 2000 Jun;105(11):1563-71 [10841515.001]
  • [Cites] Glycobiology. 2005 Dec;15(12):1257-67 [16079416.001]
  • [Cites] Nephron. 1994;66(1):21-8 [8107950.001]
  • [Cites] Pediatr Nephrol. 2003 Mar;18(3):246-53 [12644917.001]
  • [Cites] J Infect Dis. 2008 Nov 1;198(9):1398-406 [18754742.001]
  • [Cites] FEBS J. 2006 May;273(9):2064-75 [16724420.001]
  • [Cites] Kidney Int. 2002 Sep;62(3):832-45 [12164865.001]
  • [Cites] Methods Mol Med. 2003;73:197-208 [12375430.001]
  • [Cites] J Biol Chem. 1976 Dec 10;251(23):7517-20 [1002698.001]
  • [Cites] Am J Pathol. 1999 Apr;154(4):1285-99 [10233866.001]
  • [Cites] Eur J Biochem. 2004 Jan;271(2):405-17 [14717708.001]
  • [Cites] Am J Nephrol. 2005 Nov-Dec;25(6):536-40 [16179829.001]
  • [Cites] Infect Immun. 1993 Aug;61(8):3392-402 [8335369.001]
  • [Cites] J Biol Chem. 2006 Apr 14;281(15):10230-5 [16476743.001]
  • [Cites] Anal Biochem. 1995 May 1;227(1):195-200 [7668381.001]
  • [Cites] Biochim Biophys Acta. 1966 Apr 4;116(2):279-87 [5956914.001]
  • (PMID = 18365234.001).
  • [ISSN] 0948-6143
  • [Journal-full-title] Histochemistry and cell biology
  • [ISO-abbreviation] Histochem. Cell Biol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI024431; United States / PHS HHS / / T32 A1055432-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Shiga Toxins; 0 / Trihexosylceramides; 71965-57-6 / globotriaosylceramide
  •  go-up   go-down


Advertisement
4. Alder O, Cullum R, Lee S, Kan AC, Wei W, Yi Y, Garside VC, Bilenky M, Griffith M, Morrissy AS, Robertson GA, Thiessen N, Zhao Y, Chen Q, Pan D, Jones SJ, Marra MA, Hoodless PA: Hippo signaling influences HNF4A and FOXA2 enhancer switching during hepatocyte differentiation. Cell Rep; 2014 Oct 9;9(1):261-71
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cell fate acquisition is heavily influenced by direct interactions between master regulators and tissue-specific enhancers.
  • Using in vivo mouse liver development as a model, we identified thousands of enhancers that are bound by the master regulators HNF4A and FOXA2 in a differentiation-dependent manner, subject to chromatin remodeling, and associated with differentially expressed target genes.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.
  • [Cites] Nat Genet. 2000 May;25(1):25-9 [10802651.001]
  • [Cites] Physiol Genomics. 2009 Jul 9;38(2):186-95 [19417011.001]
  • [Cites] Mech Dev. 2001 Dec;109(2):183-93 [11731232.001]
  • [Cites] J Cell Sci. 2003 May 1;116(Pt 9):1775-86 [12665558.001]
  • [Cites] Nat Genet. 2003 Jul;34(3):292-6 [12808453.001]
  • [Cites] J Biol Chem. 2003 Jul 25;278(30):27495-501 [12740371.001]
  • [Cites] Mol Cell Biol. 1988 Mar;8(3):1169-78 [2452972.001]
  • [Cites] Bioinformatics. 2009 Oct 1;25(19):2605-6 [19689956.001]
  • [Cites] Curr Protoc Mol Biol. 2010 Jan;Chapter 19:Unit 19.10.1-21 [20069535.001]
  • [Cites] Nat Genet. 2010 Apr;42(4):343-7 [20208536.001]
  • [Cites] Genome Res. 2010 Aug;20(8):1037-51 [20551221.001]
  • [Cites] Genome Biol. 2010;11(8):R86 [20738864.001]
  • [Cites] Nat Methods. 2010 Oct;7(10):843-7 [20835245.001]
  • [Cites] Nature. 2011 Feb 10;470(7333):279-83 [21160473.001]
  • [Cites] Cell. 2011 Mar 4;144(5):782-95 [21376238.001]
  • [Cites] Nat Rev Genet. 2011 Apr;12(4):283-93 [21358745.001]
  • [Cites] Science. 2011 Apr 22;332(6028):458-61 [21512031.001]
  • [Cites] Nature. 2011 Jul 21;475(7356):386-9 [21562492.001]
  • [Cites] Nature. 2011 Jul 21;475(7356):390-3 [21716291.001]
  • [Cites] Genes Dev. 2011 Nov 1;25(21):2227-41 [22056668.001]
  • [Cites] Cell. 2012 Jan 20;148(1-2):72-83 [22265403.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2012 Mar 1;302(5):G493-503 [22194415.001]
  • [Cites] Nature. 2012 Aug 2;488(7409):116-20 [22763441.001]
  • [Cites] Mol Cell. 2012 Aug 10;47(3):457-68 [22771117.001]
  • [Cites] Diabetologia. 2013 Mar;56(3):542-52 [23238790.001]
  • [Cites] Genes Dev. 2013 Feb 15;27(4):355-71 [23431053.001]
  • [Cites] Hepatology. 2013 Jun;57(6):2491-501 [23315977.001]
  • [Cites] N Engl J Med. 2013 Jun 13;368(24):2266-76 [23758232.001]
  • [Cites] Biotechnol Adv. 2013 Nov 15;31(7):1085-93 [24055818.001]
  • [Cites] Stem Cells Dev. 2014 Jan 15;23(2):124-31 [24020366.001]
  • [Cites] Cell Stem Cell. 2014 Mar 6;14(3):394-403 [24582926.001]
  • [Cites] Cell Stem Cell. 2014 Mar 6;14(3):370-84 [24582927.001]
  • [Cites] Cell Stem Cell. 2014 Jun 5;14(6):838-53 [24905168.001]
  • [Cites] Cell. 2014 Jun 5;157(6):1324-38 [24906150.001]
  • [Cites] PLoS One. 2014;9(6):e100134 [24963715.001]
  • [Cites] Development. 1997 Jan;124(2):279-87 [9053305.001]
  • [Cites] Mol Cell. 1998 Jul;2(1):109-20 [9702197.001]
  • [Cites] Nature. 2005 Jun 16;435(7044):944-7 [15959514.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 30;103(22):8419-24 [16714383.001]
  • [Cites] Cell. 2006 Jun 30;125(7):1253-67 [16814713.001]
  • [Cites] Genes Dev. 2006 Aug 15;20(16):2293-305 [16912278.001]
  • [Cites] Lab Invest. 2006 Dec;86(12):1272-84 [17117158.001]
  • [Cites] Nat Methods. 2007 Aug;4(8):651-7 [17558387.001]
  • [Cites] Cell. 2007 Sep 21;130(6):1120-33 [17889654.001]
  • [Cites] Curr Biol. 2007 Dec 4;17(23):2054-60 [17980593.001]
  • [Cites] Cell. 2008 Mar 21;132(6):958-70 [18358809.001]
  • [Cites] Bioinformatics. 2008 Aug 1;24(15):1729-30 [18599518.001]
  • [Cites] Nucleic Acids Res. 2008 Aug;36(14):4549-64 [18611952.001]
  • [Cites] BMC Bioinformatics. 2009;10:48 [19192299.001]
  • [Cites] Gastroenterology. 2009 Mar;136(3):1000-11 [19185577.001]
  • [Cites] Genes Dev. 2009 Apr 1;23(7):804-9 [19339686.001]
  • [Cites] Mol Cell Biol. 2001 Feb;21(4):1393-403 [11158324.001]
  • (PMID = 25263553.001).
  • [ISSN] 2211-1247
  • [Journal-full-title] Cell reports
  • [ISO-abbreviation] Cell Rep
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE54520
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973; Canada / Canadian Institutes of Health Research / / FRN259575; United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; 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 / Foxa2 protein, mouse; 0 / Hepatocyte Nuclear Factor 4; 0 / Hnf4a protein, mouse; 135845-92-0 / Hepatocyte Nuclear Factor 3-beta; EC 2.7.11.1 / Hippo protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ NIHMS724768; NLM/ PMC4612615
  •  go-up   go-down


5. Martinez-Jimenez CP, Kyrmizi I, Cardot P, Gonzalez FJ, Talianidis I: Hepatocyte nuclear factor 4alpha coordinates a transcription factor network regulating hepatic fatty acid metabolism. Mol Cell Biol; 2010 Feb;30(3):565-77
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hes6 is identified as a novel HNF4alpha target, which in normally fed animals, together with HNF4alpha, maintains PPARgamma expression at low levels and represses several PPARalpha-regulated genes.
  • During fasting, Hes6 expression is diminished, and peroxisome proliferator-activated receptor alpha (PPARalpha) replaces the HNF4alpha/Hes6 complex on regulatory regions of target genes to activate transcription.
  • Gene expression and promoter occupancy analyses confirmed that HNF4alpha is a direct activator of the Pparalpha gene in vivo and that its expression is subject to feedback regulation by PPARalpha and Hes6 proteins.
  • [MeSH-minor] Animals. Biological Transport / physiology. Cell Line, Tumor. Gene Expression Regulation, Enzymologic / genetics. Gene Expression Regulation, Enzymologic / physiology. Humans. Mice. Mice, Inbred C57BL. Mice, Inbred CBA. Mice, Transgenic. PPAR alpha / metabolism. PPAR gamma / metabolism. Promoter Regions, Genetic / physiology. Signal Transduction / genetics. Signal Transduction / physiology. Transcriptional Activation / physiology

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Endocrinology. 2000 Nov;141(11):4021-31 [11089532.001]
  • [Cites] Annu Rev Biochem. 2008;77:289-312 [18518822.001]
  • [Cites] Mol Cell. 2008 Aug 22;31(4):531-43 [18722179.001]
  • [Cites] Cell Metab. 2008 Sep;8(3):212-23 [18762022.001]
  • [Cites] Cell Metab. 2009 Mar;9(3):228-39 [19254568.001]
  • [Cites] Mol Endocrinol. 2009 Apr;23(4):434-43 [19179483.001]
  • [Cites] Diabetes. 2009 May;58(5):1245-53 [19188435.001]
  • [Cites] EMBO J. 1990 Mar;9(3):869-78 [1690125.001]
  • [Cites] Mol Cell Biol. 2001 Nov;21(21):7320-30 [11585914.001]
  • [Cites] J Biol Chem. 2002 Apr 19;277(16):14011-9 [11834723.001]
  • [Cites] Mol Endocrinol. 2002 May;16(5):1013-28 [11981036.001]
  • [Cites] J Clin Invest. 2002 May;109(9):1125-31 [11994399.001]
  • [Cites] Cell Mol Life Sci. 2002 May;59(5):790-8 [12088279.001]
  • [Cites] Mol Cell Biochem. 2002 Oct;239(1-2):193-7 [12479585.001]
  • [Cites] J Biol Chem. 2003 Jan 3;278(1):498-505 [12401792.001]
  • [Cites] Mol Cell. 2002 Dec;10(6):1467-77 [12504020.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):4012-7 [12651943.001]
  • [Cites] J Biol Chem. 2003 Sep 5;278(36):34268-76 [12805374.001]
  • [Cites] Mol Cell Biol. 2003 Oct;23(19):6922-35 [12972610.001]
  • [Cites] Nature. 2003 Nov 13;426(6963):190-3 [14614508.001]
  • [Cites] Genes Dev. 2000 Feb 15;14(4):464-74 [10691738.001]
  • [Cites] Mol Cell. 2000 Apr;5(4):745-51 [10882110.001]
  • [Cites] J Biol Chem. 2004 Jan 23;279(4):2480-9 [14583614.001]
  • [Cites] Mol Cell. 2004 Apr 23;14(2):175-82 [15099517.001]
  • [Cites] J Biol Chem. 1994 Jul 22;269(29):18767-72 [7913466.001]
  • [Cites] Genes Dev. 1994 May 15;8(10):1224-34 [7926726.001]
  • [Cites] Mol Cell Biol. 1995 Jun;15(6):3012-22 [7539101.001]
  • [Cites] Eur J Biochem. 1997 Feb 15;244(1):1-14 [9063439.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):76-83 [9916795.001]
  • [Cites] J Clin Invest. 1999 Jun;103(11):1489-98 [10359558.001]
  • [Cites] EMBO J. 2005 Jan 26;24(2):347-57 [15616580.001]
  • [Cites] EMBO J. 2005 Jul 20;24(14):2624-33 [15973435.001]
  • [Cites] J Lipid Res. 2006 Jan;47(1):215-27 [16264197.001]
  • [Cites] Annu Rev Physiol. 2006;68:159-91 [16460270.001]
  • [Cites] Physiol Rev. 2006 Apr;86(2):465-514 [16601267.001]
  • [Cites] Cell Metab. 2006 Aug;4(2):107-10 [16890538.001]
  • [Cites] Genes Dev. 2006 Aug 15;20(16):2293-305 [16912278.001]
  • [Cites] Mol Cell Biol. 2006 Oct;26(19):7017-29 [16980607.001]
  • [Cites] Pharmacol Rev. 2006 Dec;58(4):726-41 [17132851.001]
  • [Cites] Cell Metab. 2007 Jun;5(6):415-25 [17550777.001]
  • [Cites] Cell Metab. 2007 Jun;5(6):426-37 [17550778.001]
  • [Cites] J Lipid Res. 2007 Aug;48(8):1781-91 [17485727.001]
  • [Cites] Cell Metab. 2008 Apr;7(4):302-11 [18396136.001]
  • [Cites] Mol Cell Biol. 2001 Feb;21(4):1393-403 [11158324.001]
  • (PMID = 19933841.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Fatty Acids; 0 / Hepatocyte Nuclear Factor 4; 0 / Hes6 protein, mouse; 0 / PPAR alpha; 0 / PPAR gamma; 0 / Repressor Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2812226
  •  go-up   go-down


6. Provoda CJ, Stier EM, Lee KD: Tumor cell killing enabled by listeriolysin O-liposome-mediated delivery of the protein toxin gelonin. J Biol Chem; 2003 Sep 12;278(37):35102-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Being a hydrophilic macromolecule, however, gelonin has limited access to its target subcellular compartment, the cytosol; it is effectively plasma membrane-impermeant and subject to rapid degradation within endosomes and lysosomes upon cellular uptake as it lacks the membrane-translocating capability that is typically provided by a disulfide-linked B polypeptide found in the type II toxins (e.g. ricin).
  • Moreover, treatment by direct intratumor injection into subcutaneous solid tumors of B16 melanoma in a mouse model showed that pH-sensitive liposomes containing both listeriolysin O and gelonin were more effective than control formulations in curtailing tumor growth rates.
  • [MeSH-minor] Animals. Antineoplastic Agents, Phytogenic / pharmacokinetics. Antineoplastic Agents, Phytogenic / toxicity. Bacterial Toxins / toxicity. Biological Transport. Drug Carriers. Hemolysin Proteins. Hydrogen-Ion Concentration. Mice. Mice, Inbred C57BL. Ribosome Inactivating Proteins, Type 1. Tumor Cells, Cultured

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12832408.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / F32AI010571; United States / NIGMS NIH HHS / GM / GM07767; United States / NIAID NIH HHS / AI / R01AI47173; United States / NIAID NIH HHS / AI / R29AI42084
  • [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 / Antineoplastic Agents, Phytogenic; 0 / Bacterial Toxins; 0 / Drug Carriers; 0 / Heat-Shock Proteins; 0 / Hemolysin Proteins; 0 / Liposomes; 0 / Plant Proteins; 0 / Ribosome Inactivating Proteins, Type 1; 72270-41-8 / hlyA protein, Listeria monocytogenes; 75037-46-6 / GEL protein, Gelonium multiflorum
  •  go-up   go-down


7. Kelz MB, Kuszak JR, Yang Y, Ma W, Steffen C, Al-Ghoul K, Zhang YJ, Chen J, Nestler EJ, Spector A: DeltaFosB-induced cataract. Invest Ophthalmol Vis Sci; 2000 Oct;41(11):3523-38
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Western blot analysis was performed on bitransgenic NSE-tTA, TetOp-DeltaFosB, and single-transgenic NSE-tTA control mice to determine the pattern of DeltaFosB expression within the eye.
  • RESULTS: In mice expressing DeltaFosB, cataract developed that initially appeared to be posterior subcapsular and gradually matured to involve the entire lens.
  • The development of cataracts was a direct consequence of DeltaFosB expression and was not due to the disruption of an endogenous gene by transgene integration since cataracts could be prevented by silencing expression of DeltaFosB by feeding bitransgenic animals doxycycline (Dox).
  • Moreover, cataracts were observed in bitransgenic mice derived from two independent TetOp-DeltaFosB founder lines but not in single NSE-tTA transgenic controls.
  • Cataractogenesis was not a consequence of abnormal development, because mice conceived and raised on Dox to prevent expression of DeltaFosB also were subject to formation of PSC when expression of DeltaFosB was turned on in adult animals by removing Dox.
  • By identifying DeltaFosB-regulated target genes, it should be possible to achieve a better understanding of the molecular mechanisms through which PSC is formed.
  • [MeSH-minor] Animals. Blotting, Western. Calcium / metabolism. Crystallins / metabolism. Doxycycline / pharmacology. Electrophoresis, Polyacrylamide Gel. Gene Expression Regulation / drug effects. Lens Subluxation / etiology. Mice. Mice, Inbred C57BL. Mice, Inbred ICR. Mice, Transgenic. Microscopy, Electron, Scanning. Organ Size. Pigment Epithelium of Eye / metabolism. Pigment Epithelium of Eye / pathology. Retina / metabolism. Retina / pathology. Rubidium / metabolism

  • MedlinePlus Health Information. consumer health - Cataract.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOXYCYCLINE .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11006248.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [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 / Crystallins; 0 / Proto-Oncogene Proteins c-fos; MLT4718TJW / Rubidium; N12000U13O / Doxycycline; SY7Q814VUP / Calcium
  •  go-up   go-down


8. Mathew B, Lennon FE, Siegler J, Mirzapoiazova T, Mambetsariev N, Sammani S, Gerhold LM, LaRiviere PJ, Chen CT, Garcia JG, Salgia R, Moss J, Singleton PA: The novel role of the mu opioid receptor in lung cancer progression: a laboratory investigation. Anesth Analg; 2011 Mar;112(3):558-67
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The possibility that μ opioid agonists can influence cancer recurrence is a subject of recent interest.
  • LLC cells were treated with the peripheral opioid antagonist methylnaltrexone (MNTX) or MOR shRNA and evaluated for proliferation, invasion, and soft agar colony formation in vitro and primary tumor growth and lung metastasis in C57BL/6 and MOR knockout mice using VisEn fluorescence mediated tomography imaging and immunohistochemical analysis.
  • RESULTS: We provide several lines of evidence that the MOR may be a potential target for lung cancer, a disease with high mortality and few treatment options.
  • Injection of MOR silenced LLC lead to a ∼65% reduction in mouse lung metastasis.
  • In addition, MOR knockout mice do not develop significant tumors when injected with LLC in comparison with wild-type controls.
  • CONCLUSIONS: Taken together, our data suggest a possible direct effect of opiates on lung cancer progression, and provide a plausible explanation for the epidemiologic findings.
  • [MeSH-minor] Animals. Cell Line. Cell Line, Tumor. Female. Humans. Mice. Mice, Inbred C57BL. Mice, Knockout. Neoplasm Invasiveness / pathology. Xenograft Model Antitumor Assays


9. Ooi JY, Tuano NK, Rafehi H, Gao XM, Ziemann M, Du XJ, El-Osta A: HDAC inhibition attenuates cardiac hypertrophy by acetylation and deacetylation of target genes. Epigenetics; 2015;10(5):418-30
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HDAC inhibition attenuates cardiac hypertrophy by acetylation and deacetylation of target genes.
  • Pharmacological histone deacetylase (HDAC) inhibitors attenuate pathological cardiac remodeling and hypertrophic gene expression; yet, the direct histone targets remain poorly characterized.
  • Since the inhibition of HDAC activity is associated with suppressing hypertrophy, we hypothesized histone acetylation would target genes implicated in cardiac remodeling.
  • Increased histone acetylation was observed on the promoters of NFκB target genes (Icam1, Vcam1, Il21r, Il6ra, Ticam2, Cxcl10) consistent with gene activation in the hypertrophied heart.
  • Surprisingly, TSA attenuated pressure overload-induced cardiac hypertrophy and the suppression of NFκB target genes by broad histone deacetylation.
  • Our results suggest a mechanism for cardioprotection subject to histone deacetylation as a previously unknown target, implicating the importance of inflammation by pharmacological HDAC inhibition.
  • The results of this study provides a framework for HDAC inhibitor function in the heart and argues the long held views of acetylation is subject to more flexibility than previously thought.
  • [MeSH-minor] Animals. Aorta / surgery. Gene Expression Regulation / drug effects. Histones / metabolism. Male. Mice, Inbred C57BL. Myocardium / metabolism. NF-kappa B / metabolism

  • figshare. supplemental materials - Supporting Data and Materials for the article .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Brief Bioinform. 2013 Mar;14(2):144-61 [22908213.001]
  • [Cites] Proc Natl Acad Sci U S A. 2013 Dec 10;110(50):20164-9 [24284169.001]
  • [Cites] Nucleic Acids Res. 2014 Jan;42(2):790-803 [24137001.001]
  • [Cites] Circulation. 2001 Feb 27;103(8):1044-7 [11222463.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2000 Feb;278(2):H412-9 [10666070.001]
  • [Cites] Genome Res. 2014 Aug;24(8):1271-84 [24732587.001]
  • [Cites] J Clin Invest. 2005 Mar;115(3):538-46 [15765135.001]
  • [Cites] Mol Cell. 2005 Jun 10;18(6):735-48 [15949447.001]
  • [Cites] Cell. 2005 Aug 26;122(4):517-27 [16122420.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Circulation. 2006 Jan 3;113(1):51-9 [16380549.001]
  • [Cites] Curr Opin Genet Dev. 2006 Apr;16(2):125-36 [16503131.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2006 Jun;290(6):H2351-61 [16415074.001]
  • [Cites] Circulation. 2006 Jun 6;113(22):2579-88 [16735673.001]
  • [Cites] Novartis Found Symp. 2006;274:3-12; discussion 13-9, 152-5, 272-6 [17019803.001]
  • [Cites] J Biol Chem. 2007 Feb 16;282(7):4408-16 [17166833.001]
  • [Cites] Genome Biol. 2008;9(9):R137 [18798982.001]
  • [Cites] Science. 2001 Aug 10;293(5532):1074-80 [11498575.001]
  • [Cites] Genome Res. 2002 Jun;12(6):996-1006 [12045153.001]
  • [Cites] Cell. 2002 Aug 23;110(4):479-88 [12202037.001]
  • [Cites] Curr Opin Cell Biol. 2002 Dec;14(6):763-72 [12473352.001]
  • [Cites] Nat Genet. 2007 Mar;39(3):311-8 [17277777.001]
  • [Cites] Nat Med. 2007 Mar;13(3):324-31 [17322895.001]
  • [Cites] Genome Res. 2007 Jun;17(6):708-19 [17567991.001]
  • [Cites] J Mol Biol. 2008 Jan 18;375(3):637-49 [18037434.001]
  • [Cites] Trends Genet. 2008 Mar;24(3):133-41 [18262675.001]
  • [Cites] Nat Genet. 2008 Jul;40(7):897-903 [18552846.001]
  • [Cites] Cardiovasc Res. 2008 Dec 1;80(3):416-24 [18697792.001]
  • [Cites] Curr Opin Cell Biol. 2003 Apr;15(2):172-83 [12648673.001]
  • [Cites] J Biol Chem. 2003 Aug 1;278(31):28930-7 [12761226.001]
  • [Cites] J Clin Invest. 2003 Sep;112(6):863-71 [12975471.001]
  • [Cites] Trends Genet. 2004 Apr;20(4):206-13 [15041175.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 11;101(19):7357-62 [15123803.001]
  • [Cites] Novartis Found Symp. 2004;259:132-41; discussion 141-5, 163-9 [15171251.001]
  • [Cites] Nat Genet. 2004 Aug;36(8):900-5 [15247917.001]
  • [Cites] Nucleic Acids Res. 1984 Jan 25;12(2):1087-100 [6546444.001]
  • [Cites] Am J Physiol. 1991 Jan;260(1 Pt 2):H73-9 [1825154.001]
  • [Cites] Nature. 1997 Sep 18;389(6648):251-60 [9305837.001]
  • [Cites] J Clin Invest. 1997 Nov 1;100(9):2362-70 [9410916.001]
  • [Cites] Circulation. 1999 Jun 29;99(25):3224-6 [10385494.001]
  • [Cites] N Engl J Med. 1999 Oct 21;341(17):1276-83 [10528039.001]
  • [Cites] J Mol Cell Cardiol. 2004 Nov;37(5):979-87 [15522275.001]
  • [Cites] Bioinformatics. 2009 Jul 15;25(14):1754-60 [19451168.001]
  • [Cites] Science. 2009 Aug 14;325(5942):834-40 [19608861.001]
  • [Cites] Nat Rev Genet. 2009 Oct;10(10):669-80 [19736561.001]
  • [Cites] Cardiovasc Res. 2009 Dec 1;84(3):416-24 [19620128.001]
  • [Cites] Bioinformatics. 2010 Mar 15;26(6):841-2 [20110278.001]
  • [Cites] Br J Pharmacol. 2010 Apr;159(7):1408-17 [20180942.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2010 Jun;298(6):H2154-63 [20382965.001]
  • [Cites] Heart Fail Rev. 2010 Jul;15(4):331-41 [19363700.001]
  • [Cites] Nature. 2010 Jul 1;466(7302):62-7 [20596014.001]
  • [Cites] Expert Opin Investig Drugs. 2010 Sep;19(9):1049-66 [20687783.001]
  • [Cites] Hypertension. 2010 Sep;56(3):437-44 [20679181.001]
  • [Cites] Pharmacol Ther. 2010 Oct;128(1):191-227 [20438756.001]
  • [Cites] Cardiovasc Res. 2011 Jan 1;89(1):129-38 [20797985.001]
  • [Cites] Nucleic Acids Res. 2011 Jan;39(Database issue):D871-5 [21037257.001]
  • [Cites] Proc Natl Acad Sci U S A. 2011 Mar 8;108(10):4123-8 [21367693.001]
  • [Cites] Circ Res. 2011 Apr 29;108(9):1122-32 [21527742.001]
  • [Cites] Mol Med. 2011 May-Jun;17(5-6):434-41 [21267510.001]
  • [Cites] Epigenetics. 2011 Jun;6(6):760-8 [21586902.001]
  • [Cites] Handb Exp Pharmacol. 2011;206:57-78 [21879446.001]
  • [Cites] J Mol Cell Cardiol. 2011 Oct;51(4):491-6 [21108947.001]
  • [Cites] PLoS One. 2012;7(3):e33453 [22479401.001]
  • [Cites] J Biol Chem. 2013 Jan 25;288(4):2546-58 [23229551.001]
  • (PMID = 25941940.001).
  • [ISSN] 1559-2308
  • [Journal-full-title] Epigenetics
  • [ISO-abbreviation] Epigenetics
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE63590
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Hydroxamic Acids; 0 / NF-kappa B; 3X2S926L3Z / trichostatin A; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ PMC4622459
  • [Keywords] NOTNLM ; ANP, Atrial natriuretic peptide / BNP, Brain natriuretic peptide / BW, Body Weight / ChIP, Chromatin Immunoprecipitation / Ct, threshold cycle number / Cxcl10, Chemokine (C-X-C Motif) ligand 10 / ENCODE, Encyclopedia of DNA Elements Consortium / FDR, False Discovery Rate / FS, Fractional Shortening / GAIIx, Genome Analyzer IIx / HDAC inhibitor / HDAC, Histone deacetylase / Icam1, Intercellular adhesion molecule 1 / Il21r, Interleukin-21 receptor / Il6ra, Interleukin-6 receptor / LV, Left Ventricle / LVDd, Left Ventricular Diastolic Dimension / LVH, Left Ventricle Hypertrophy / MACs, Model-based Analysis of ChIP-seq / NES, normalized enrichment score / NFκB, Nuclear factor of kappa light polypeptide gene enhancer in B-cells / NGS, Next Generation Sequencing / SEM, Standard Error of the Mean / Serca2a, Sarcoplasmic reticulum Ca2+ ATPase / TAC veh, TAC vehicle / TAC, Transverse Aortic Constriction / TF, transcription factor / TL, Tibia Length / TSA, Trichostatin A / TSS, Transcription Start Site / Ticam2, Toll-like receptor adaptor molecule 2 / Traf3, TNF receptor-associated factor 3 / UTR, Untranslated region / Vcam1, Vascular cell adhesion molecule 1 / cDNA, complementary DNA / cardiac hypertrophy / chromatin / epigenetics / histone acetylation / next generation sequencing / α/βMHC, Alpha/Beta myosin heavy chain
  •  go-up   go-down






Advertisement