Disruption of the cyclic AMP phosphodiesterase-4 (PDE4)-HSP20 complex attenuates the β-agonist induced hypertrophic response in cardiac myocytes.

@article{Sin2011DisruptionOT,
  title={Disruption of the cyclic AMP phosphodiesterase-4 (PDE4)-HSP20 complex attenuates the β-agonist induced hypertrophic response in cardiac myocytes.},
  author={Yuan Yan Sin and Helen V Edwards and Xiaohai Li and Jonathan Paul Day and Frank Christian and Allan J. Dunlop and David R Adams and Manuela Zaccolo and Miles D Houslay and George S Baillie},
  journal={Journal of molecular and cellular cardiology},
  year={2011},
  volume={50 5},
  pages={872-83}
}
The small heat shock protein HSP20 is known to be cardioprotective during times of stress and the mechanism underlying its protective abilities depends on its phosphorylation on Ser16 by PKA (protein kinase A). Although the external stimuli that trigger Ser16 phosphorylation have been well studied, the events that modulate spatial and temporal control of this modification remain to be clarified. Here, we report that inhibition of cAMP phosphodiesterase-4 (PDE4) induces the phosphorylation of… CONTINUE READING

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