MYH10 for PKP2-mutant arrhythmogenic cardiomyopathy

Activation or overexpression of the non-muscle myosin protein MYH10 could help treat arrhythmogenic cardiomyopathy caused by gain-of-function mutations in the desmosomal protein PKP2, a MYH10 interaction partner, by improving actin organization and increasing cell stiffness.

Mass spectrometry, co-immunoprecipitation and fluorescence microscopy experiments showed a disease-causing PKP2 mutation increased binding to MYH10 compared with wild-type PKP2, and induced PKP2 mislocalization from the plasma membrane to the cytosol. ...