Histone deacetylase 5
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Histone deacetylase 5, also known as HDAC5, is a human gene.[1]
Histones play a critical role in transcriptional regulation, cell cycle progression, and developmental events. Histone acetylation/deacetylation alters chromosome structure and affects transcription factor access to DNA. The protein encoded by this gene belongs to the class II histone deacetylase/acuc/apha family. It possesses histone deacetylase activity 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.[1]
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- Scanlan MJ, Chen YT, Williamson B, et al. (1998). "Characterization of human colon cancer antigens recognized by autologous antibodies.". Int. J. Cancer 76 (5): 652–8. PMID 9610721.
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- Huang EY, Zhang J, Miska EA, et al. (2000). "Nuclear receptor corepressors partner with class II histone deacetylases in a Sin3-independent repression pathway.". Genes Dev. 14 (1): 45–54. PMID 10640275.
- Lemercier C, Verdel A, Galloo B, et al. (2000). "mHDA1/HDAC5 histone deacetylase interacts with and represses MEF2A transcriptional activity.". J. Biol. Chem. 275 (20): 15594–9. doi: . PMID 10748098.
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- Mahlknecht U, Schnittger S, Ottmann OG, et al. (2000). "Chromosomal organization and localization of the human histone deacetylase 5 gene (HDAC5).". Biochim. Biophys. Acta 1493 (3): 342–8. PMID 11018260.
- Zhang CL, McKinsey TA, Lu JR, Olson EN (2001). "Association of COOH-terminal-binding protein (CtBP) and MEF2-interacting transcription repressor (MITR) contributes to transcriptional repression of the MEF2 transcription factor.". J. Biol. Chem. 276 (1): 35–9. doi: . PMID 11022042.
- McKinsey TA, Zhang CL, Lu J, Olson EN (2000). "Signal-dependent nuclear export of a histone deacetylase regulates muscle differentiation.". Nature 408 (6808): 106–11. doi: . PMID 11081517.
- McKinsey TA, Zhang CL, Olson EN (2001). "Activation of the myocyte enhancer factor-2 transcription factor by calcium/calmodulin-dependent protein kinase-stimulated binding of 14-3-3 to histone deacetylase 5.". Proc. Natl. Acad. Sci. U.S.A. 97 (26): 14400–5. doi: . PMID 11114197.
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- McKinsey TA, Zhang CL, Olson EN (2001). "Identification of a signal-responsive nuclear export sequence in class II histone deacetylases.". Mol. Cell. Biol. 21 (18): 6312–21. PMID 11509672.
- Ozawa Y, Towatari M, Tsuzuki S, et al. (2001). "Histone deacetylase 3 associates with and represses the transcription factor GATA-2.". Blood 98 (7): 2116–23. PMID 11567998.
- Potter GB, Beaudoin GM, DeRenzo CL, et al. (2001). "The hairless gene mutated in congenital hair loss disorders encodes a novel nuclear receptor corepressor.". Genes Dev. 15 (20): 2687–701. doi: . PMID 11641275.
- Fischle W, Dequiedt F, Hendzel MJ, et al. (2002). "Enzymatic activity associated with class II HDACs is dependent on a multiprotein complex containing HDAC3 and SMRT/N-CoR.". Mol. Cell 9 (1): 45–57. PMID 11804585.
- Lemercier C, Brocard MP, Puvion-Dutilleul F, et al. (2002). "Class II histone deacetylases are directly recruited by BCL6 transcriptional repressor.". J. Biol. Chem. 277 (24): 22045–52. doi: . PMID 11929873.
- Huang Y, Tan M, Gosink M, et al. (2002). "Histone deacetylase 5 is not a p53 target gene, but its overexpression inhibits tumor cell growth and induces apoptosis.". Cancer Res. 62 (10): 2913–22. PMID 12019172.
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This article incorporates text from the United States National Library of Medicine, which is in the public domain.