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The anti-apoptotic protein HAX-1 interacts with PLN and enhances its inhibitory effects on SERCA2a and contractility. PKA phosphorylation of PLN or ablation of HAX-1 abolish the inhibition of HAX-1 on PLN/SERCA and Ca-cycling. Accordingly, overexpression of HAX-1 increases PLN inhibition and depresses contractility.
