Enhanced binding of calmodulin to RyR2 corrects arrhythmogenic channel disorder in CPVT-associated myocytes

Several disorders in the RyR channel function characteristic of the CPVT-mutant cells (increased spontaneous Ca2+ leak, delayed afterdepolarization, triggered activity, Ca2+ spark frequency, spontaneous Ca2+ transients) can be corrected to a normal function by increasing the affinity of CaM binding to the RyR.