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Partial replacement of cardiac troponin I with a non-phosphorylatable mutant at serines 43/45 attenuates the contractile dysfunction associated with PKCε phosphorylation

Cardiac MuscleCardiomyopathyMolecular PhysiologySignal TransductionMedicinePartial ReplacementPhysiologyContractile DysfunctionCardiovascular PhysiologyCardiac TroponinCell BiologyCell SignalingProtein Phosphorylation