Rama Reddy Goluguri

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

This study investigates how HCM mutations Y115H and E497D disrupt the folded-back state of human beta-cardiac myosin, leading to hypercontractility by destabilizing the OFF-state.

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

The paper develops a FRET assay to directly quantify the IHM state of human β-cardiac myosin and shows how mutations and perturbations affect its stability.