Aminah Dawood

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

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.