Abstract Aims The aim of the present study was to determine the function and the role of the scaffold protein AKAP, tethering cAMP dependent protein kinase A to the outer wall of mitochondria, in neonatal ventricular myocytes and the heart. Methods and results Competitive peptides displacing AKAP from mitochondria in the tissue and in the cells were used to investigate the role of AKAP in mitochondrial function, reactive oxygen species ROS generation, and cell survival. Displacement of AKAP from mitochondria by synthetic peptides triggers the death program in cardiomyocytes.
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