Abstract
Chronic protein kinase C (PKC) activity is routinely linked to cardiac dysfunction and heart failure. PKC targets the thin filament molecular switch protein, cardiac troponin I (cTnI), at multiple clusters of residues, including cTnI S43/45. Our work tests the idea that phosphorylation of cTnI S43/45 diminishes cardiac function and initiates progressive heart failure. To test this idea, our laboratory generated mice with cardiac-specific phospho-mimetic cTnI S43/45D (SD) replacement of endogenous cTnI.
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