Divya Pathak

This study shows that the E525K β-myosin mutation reduces cardiomyocyte contraction without altering crossbridge cycling, through structural and computational analysis.

This study shows that myosin inhibition with mavacamten is effective in treating HCM caused by both truncating and missense variants in MYBPC3, despite different pathomechanisms.

This paper studies the G768R mutation in cardiac myosin, showing it increases the duty ratio to >60%, leading to hypercontractility and impaired relaxation.

This study investigates how the G256E HCM mutation affects myosin function by altering nucleotide handling, leading to prolonged relaxation and contributing to hypertrophic cardiomyopathy.

This study investigates the effects of the MYH7 G256E mutation on myosin function across multiple scales, finding increased hypercontractility and mitochondrial respiration.