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Research Article Free access | 10.1172/JCI119755
Department of Medicine, Albert Einstein College of Medicine, New York, NY 10461, USA.
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Department of Medicine, Albert Einstein College of Medicine, New York, NY 10461, USA.
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Department of Medicine, Albert Einstein College of Medicine, New York, NY 10461, USA.
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Department of Medicine, Albert Einstein College of Medicine, New York, NY 10461, USA.
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Department of Medicine, Albert Einstein College of Medicine, New York, NY 10461, USA.
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Department of Medicine, Albert Einstein College of Medicine, New York, NY 10461, USA.
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Published November 1, 1997 - More info
Protein kinase C (PKC) activation in the heart has been linked to a hypertrophic phenotype and to processes that influence contractile function. To establish whether PKC activation is sufficient to induce an abnormal phenotype, PKCbeta was conditionally expressed in cardiomyocytes of transgenic mice. Transgene expression in adults caused mild and progressive ventricular hypertrophy associated with impaired diastolic relaxation, whereas expression in newborns caused sudden death associated with marked abnormalities in the regulation of intracellular calcium. Thus, the PKC signaling pathway in cardiocytes has different effects depending on the timing of expression and, in the adult, is sufficient to induce pathologic hypertrophy.