CAMK2G and myocardial infarction: While phosphorylation of the MCU by CaMKII was not shown to occur in vivo, a CaMKII-dependent change in the function of the MCU was evidenced by data demonstrating that a CaMKII inhibitory peptide targeted to the mitochondria diminished mitochondrial Ca2+ uptake and inhibited apoptosis in mice subjected to myocardial infarction and I/R injury.