FIGURE 1.

Schematic representation of the CaMKII structure/function relationship in the heart. Under basal conditions, the kinase is autoinhibited due to interaction between the regulatory and catalytic domains. Direct activation occurs when Ca²⁺/CaM binds to CaMKII, while subsequent post-translational modification (PTM) results in autonomous kinase activity. Protein interactions with CaMKII autonomously activate CaMKII in the brain but have not yet been demonstrated in the heart. Note that the size of each region is not to scale and will vary by isoform and splice variant of CaMKII.