This editorial highlights preclinical findings that CaMKII delta C phosphorylates RyR2 to decrease local Ca2+ release events in rat cardiomyocytes.
he multifunctional Ca 2 /calmodulin-dependent protein kinase II (CaMKII) modulates cardiac muscle function by regulating Ca 2 transport proteins and nuclear signaling molecules. Aberrant activity of CaMKII is implicated in heart disease. In this issue, Yang et al 1 report that acute overexpression of constitutively active splice variant CaMKII C phosphorylates the cardiac ryanodine receptor ion channel (RyR2) to decrease the rate of occurrence of local Ca 2 release events (Ca 2 sparks) and Ca 2 waves in cultured rat cardiomyocytes. A dominant negative form of CaMKII C was shown to have opposite effects.
No takes yet. Share an insight, caveat, or question.
Yamaguchi et al. (2007) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: