Key result
Treatment of cardiomyocytes with Src-activated PKCdelta leads to depressed maximum tension and cross-bridge kinetics, attributable to a dominant effect of cTnI-Thr144 phosphorylation.
Population
Detergent-extracted single cardiomyocytes
Comparison
Treatment with Src-activated PKCdelta vs Treatment with lipid-activated PKCdelta
Design
Preclinical
Authors
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Src-PKCδ-cTnI signaling may modulate contractility; leaves open its relevance to human HF or therapeutic targeting.
Tyrosine phosphorylation of PKCdelta by Src alters its substrate specificity on cardiac troponin I, providing a mechanism for stimulus-specific control of cardiac mechanics.
Sumandea et al. (2008) studied this question. Src-activated PKCdelta vs. lipid-activated PKCdelta was evaluated on Cardiac mechanics (tension and cross-bridge kinetics). Treatment of cardiomyocytes with Src-activated PKCdelta leads to depressed maximum tension and cross-bridge kinetics, attributable to a dominant effect of cTnI-Thr144 phosphorylation.
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