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Gene Review

Hdac5  -  histone deacetylase 5

Rattus norvegicus

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Disease relevance of Hdac5

  • Here, we demonstrate that the antihypertrophic chromatin-modifying enzyme histone deacetylase 5 (HDAC5) is shuttled out of the cardiomyocyte nucleus via a CRM1-mediated pathway in response to diverse signals for hypertrophy [1].

High impact information on Hdac5


  1. The CRM1 nuclear export receptor controls pathological cardiac gene expression. Harrison, B.C., Roberts, C.R., Hood, D.B., Sweeney, M., Gould, J.M., Bush, E.W., McKinsey, T.A. Mol. Cell. Biol. (2004) [Pubmed]
  2. G betagamma binds histone deacetylase 5 (HDAC5) and inhibits its transcriptional co-repression activity. Spiegelberg, B.D., Hamm, H.E. J. Biol. Chem. (2005) [Pubmed]
  3. Inactivation of the myocyte enhancer factor-2 repressor histone deacetylase-5 by endogenous Ca(2+) //calmodulin-dependent kinase II promotes depolarization-mediated cerebellar granule neuron survival. Linseman, D.A., Bartley, C.M., Le, S.S., Laessig, T.A., Bouchard, R.J., Meintzer, M.K., Li, M., Heidenreich, K.A. J. Biol. Chem. (2003) [Pubmed]
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