Protein kinases C and D mediate agonist-dependent cardiac hypertrophy through nuclear export of histone deacetylase 5.

@article{Vega2004ProteinKC,
  title={Protein kinases C and D mediate agonist-dependent cardiac hypertrophy through nuclear export of histone deacetylase 5.},
  author={R. Barrientos Vega and Brooke C. Harrison and Eric Meadows and Charles Russell Roberts and Philip J. Papst and Eric N Olson and Timothy A McKinsey},
  journal={Molecular and cellular biology},
  year={2004},
  volume={24 19},
  pages={
          8374-85
        }
}
A variety of stress signals stimulate cardiac myocytes to undergo hypertrophy. Persistent cardiac hypertrophy is associated with elevated risk for the development of heart failure. Recently, we showed that class II histone deacetylases (HDACs) suppress cardiac hypertrophy and that stress signals neutralize this repressive function by triggering phosphorylation- and CRM1-dependent nuclear export of these chromatin-modifying enzymes. However, the identities of cardiac HDAC kinases have remained… CONTINUE READING
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