In vivo phosphorylation of cardiac troponin I by protein kinase Cbeta2 decreases cardiomyocyte calcium responsiveness and contractility in transgenic mouse hearts.

@article{Takeishi1998InVP,
  title={In vivo phosphorylation of cardiac troponin I by protein kinase Cbeta2 decreases cardiomyocyte calcium responsiveness and contractility in transgenic mouse hearts.},
  author={Yasuchika Takeishi and Gavin Chu and Donald M Kirkpatrick and Zhi-wei Li and Hisao Wakasaki and Evangelia G Kranias and George L King and R. W. Smith A. Walsh},
  journal={The Journal of clinical investigation},
  year={1998},
  volume={102 1},
  pages={72-8}
}
Recently, it has been reported that the protein kinase C (PKC) beta isoform plays a critical role in the development of hypertrophy and heart failure. The purpose of the present study was to clarify the mechanism by which activation of PKCbeta led to depressed cardiac function. Thus, we used a PKCbeta2 overexpressing mouse, an animal model of heart failure, to examine mechanical properties and Ca2+ signals of isolated left ventricular cardiomyocytes. The percentage of shortening, rate of… CONTINUE READING

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