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Histone deacetylase 5

From Wikipedia, the free encyclopedia
HDAC5
Identifiers
AliasesHDAC5,HD5, NY-CO-9, histone deacetylase 5
External IDsOMIM:605315;MGI:1333784;HomoloGene:3995;GeneCards:HDAC5;OMA:HDAC5 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001015053
NM_005474
NM_139205
NM_001382393

RefSeq (protein)

NP_001015053
NP_005465
NP_001369322

n/a

Location (UCSC)Chr 17: 44.08 – 44.12 MbChr 11: 102.19 – 102.23 Mb
PubMedsearch[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Histone deacetylase 5is anenzymethat in humans is encoded by theHDAC5gene.[5][6][7]

Function

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Histonesplay a critical role in transcriptional regulation, cell cycle progression, and developmental events. Histone acetylation/deacetylation alterschromosomestructure and affectstranscription factoraccess to DNA. The protein encoded by this gene belongs to the class II histone deacetylase/acuc/apha family. It possesseshistone deacetylaseactivity and represses transcription when tethered to a promoter. It coimmunoprecipitates only with HDAC3 family member and might form multicomplex proteins. It also interacts with myocyte enhancer factor-2 (MEF2) proteins, resulting in repression of MEF2-dependent genes. This gene is thought to be associated with colon cancer. Two transcript variants encoding different isoforms have been found for this gene.[7]

AMP-activated protein kinaseregulation of the glucose transporterGLUT4occurs byphosphorylationof HDAC5.[8]

HDAC5 is involved inmemory consolidationand suggests that development of more selectiveHDAC inhibitorsfor the treatment ofAlzheimer's diseaseshould avoid targeting HDAC5.[9]Its function can be effectively examined by siRNA knockdown based on an independent validation.[10]

HDAC5 overexpression inurothelialcarcinoma cell lines inhibits long-term proliferation but can promote epithelial-to-mesenchymal transition (EMT)[11]

Interactions

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Histone deacetylase 5 has been shown tointeractwith:

See also

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References

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  1. ^abcGRCh38: Ensembl release 89: ENSG00000108840Ensembl,May 2017
  2. ^abcGRCm38: Ensembl release 89: ENSMUSG00000008855Ensembl,May 2017
  3. ^"Human PubMed Reference:".National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^"Mouse PubMed Reference:".National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^abGrozinger CM, Hassig CA, Schreiber SL (April 1999)."Three proteins define a class of human histone deacetylases related to yeast Hda1p".Proceedings of the National Academy of Sciences of the United States of America.96(9): 4868–73.Bibcode:1999PNAS...96.4868G.doi:10.1073/pnas.96.9.4868.PMC21783.PMID10220385.
  6. ^Scanlan MJ, Chen YT, Williamson B, Gure AO, Stockert E, Gordan JD, et al. (May 1998). "Characterization of human colon cancer antigens recognized by autologous antibodies".International Journal of Cancer.76(5): 652–8.doi:10.1002/(SICI)1097-0215(19980529)76:5<652::AID-IJC7>3.0.CO;2-P.PMID9610721.S2CID916155.
  7. ^ab"Entrez Gene: HDAC5 histone deacetylase 5".
  8. ^McGee SL, van Denderen BJ, Howlett KF, Mollica J, Schertzer JD, Kemp BE, Hargreaves M (April 2008)."AMP-activated protein kinase regulates GLUT4 transcription by phosphorylating histone deacetylase 5".Diabetes.57(4): 860–7.doi:10.2337/db07-0843.PMID18184930.S2CID17274354.
  9. ^Agis-Balboa RC, Pavelka Z, Kerimoglu C, Fischer A (January 2013). "Loss of HDAC5 impairs memory function: implications for Alzheimer's disease".Journal of Alzheimer's Disease.33(1): 35–44.doi:10.3233/JAD-2012-121009.hdl:2434/223089.PMID22914591.
  10. ^Munkácsy G, Sztupinszki Z, Herman P, Bán B, Pénzváltó Z, Szarvas N, Győrffy B (September 2016)."Validation of RNAi Silencing Efficiency Using Gene Array Data shows 18.5% Failure Rate across 429 Independent Experiments".Molecular Therapy: Nucleic Acids.5(9): e366.doi:10.1038/mtna.2016.66.PMC5056990.PMID27673562.
  11. ^Jaguva Vasudevan AA, Hoffmann MJ, Beck ML, Poschmann G, Petzsch P, Wiek C, et al. (April 2019)."HDAC5 Expression in Urothelial Carcinoma Cell Lines Inhibits Long-Term Proliferation but Can Promote Epithelial-to-Mesenchymal Transition".International Journal of Molecular Sciences.20(9): 2135.doi:10.3390/ijms20092135.PMC6539474.PMID31052182.
  12. ^abLemercier C, Brocard MP, Puvion-Dutilleul F, Kao HY, Albagli O, Khochbin S (June 2002)."Class II histone deacetylases are directly recruited by BCL6 transcriptional repressor".The Journal of Biological Chemistry.277(24): 22045–52.doi:10.1074/jbc.M201736200.PMID11929873.
  13. ^Zhang CL, McKinsey TA, Olson EN (October 2002)."Association of class II histone deacetylases with heterochromatin protein 1: potential role for histone methylation in control of muscle differentiation".Molecular and Cellular Biology.22(20): 7302–12.doi:10.1128/MCB.22.20.7302-7312.2002.PMC139799.PMID12242305.
  14. ^Watamoto K, Towatari M, Ozawa Y, Miyata Y, Okamoto M, Abe A, et al. (December 2003). "Altered interaction of HDAC5 with GATA-1 during MEL cell differentiation".Oncogene.22(57): 9176–84.doi:10.1038/sj.onc.1206902.PMID14668799.S2CID24491249.
  15. ^abZhang J, Kalkum M, Chait BT, Roeder RG (March 2002)."The N-CoR-HDAC3 nuclear receptor corepressor complex inhibits the JNK pathway through the integral subunit GPS2".Molecular Cell.9(3): 611–23.doi:10.1016/S1097-2765(02)00468-9.PMID11931768.
  16. ^Fischle W, Dequiedt F, Hendzel MJ, Guenther MG, Lazar MA, Voelter W, Verdin E (January 2002). "Enzymatic activity associated with class II HDACs is dependent on a multiprotein complex containing HDAC3 and SMRT/N-CoR".Molecular Cell.9(1): 45–57.doi:10.1016/S1097-2765(01)00429-4.hdl:11858/00-001M-0000-002C-9FF9-9.PMID11804585.
  17. ^Grozinger CM, Schreiber SL (July 2000)."Regulation of histone deacetylase 4 and 5 and transcriptional activity by 14-3-3-dependent cellular localization".Proceedings of the National Academy of Sciences of the United States of America.97(14): 7835–40.Bibcode:2000PNAS...97.7835G.doi:10.1073/pnas.140199597.PMC16631.PMID10869435.
  18. ^Koipally J, Georgopoulos K (August 2002)."A molecular dissection of the repression circuitry of Ikaros".The Journal of Biological Chemistry.277(31): 27697–705.doi:10.1074/jbc.M201694200.PMID12015313.
  19. ^Lemercier C, Verdel A, Galloo B, Curtet S, Brocard MP, Khochbin S (May 2000)."mHDA1/HDAC5 histone deacetylase interacts with and represses MEF2A transcriptional activity".The Journal of Biological Chemistry.275(20): 15594–9.doi:10.1074/jbc.M908437199.PMID10748098.
  20. ^Castet A, Boulahtouf A, Versini G, Bonnet S, Augereau P, Vignon F, et al. (2004)."Multiple domains of the Receptor-Interacting Protein 140 contribute to transcription inhibition".Nucleic Acids Research.32(6): 1957–66.doi:10.1093/nar/gkh524.PMC390375.PMID15060175.
  21. ^abHuang EY, Zhang J, Miska EA, Guenther MG, Kouzarides T, Lazar MA (January 2000)."Nuclear receptor corepressors partner with class II histone deacetylases in a Sin3-independent repression pathway".Genes & Development.14(1): 45–54.doi:10.1101/gad.14.1.45.PMC316335.PMID10640275.
  22. ^Vega RB, Harrison BC, Meadows E, Roberts CR, Papst PJ, Olson EN, McKinsey TA (October 2004)."Protein kinases C and D mediate agonist-dependent cardiac hypertrophy through nuclear export of histone deacetylase 5".Molecular and Cellular Biology.24(19): 8374–85.doi:10.1128/MCB.24.19.8374-8385.2004.PMC516754.PMID15367659.
  23. ^Chauchereau A, Mathieu M, de Saintignon J, Ferreira R, Pritchard LL, Mishal Z, et al. (November 2004). "HDAC4 mediates transcriptional repression by the acute promyelocytic leukaemia-associated protein PLZF".Oncogene.23(54): 8777–84.doi:10.1038/sj.onc.1208128.PMID15467736.S2CID26092755.

Further reading

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This article incorporates text from theUnited States National Library of Medicine,which is in thepublic domain.