Signal-dependent repression of DUSP5 by class I HDACs controls nuclear ERK activity and cardiomyocyte hypertrophy.

@article{Ferguson2013SignaldependentRO,
  title={Signal-dependent repression of DUSP5 by class I HDACs controls nuclear ERK activity and cardiomyocyte hypertrophy.},
  author={Bradley S Ferguson and Brooke C. Harrison and Mark Y Jeong and Brian G. Reid and Michael F. Wempe and Florence F Wagner and Edward B Holson and Timothy A McKinsey},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2013},
  volume={110 24},
  pages={9806-11}
}
Cardiac hypertrophy is a strong predictor of morbidity and mortality in patients with heart failure. Small molecule histone deacetylase (HDAC) inhibitors have been shown to suppress cardiac hypertrophy through mechanisms that remain poorly understood. We report that class I HDACs function as signal-dependent repressors of cardiac hypertrophy via inhibition of the gene encoding dual-specificity phosphatase 5 (DUSP5) DUSP5, a nuclear phosphatase that negatively regulates prohypertrophic signaling… CONTINUE READING
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