Mutations in myosin can lead to conditions like hypertrophic cardiomyopathy (HCM) by altering structure or chemo-mechanical function. Here, the authors use molecular dynamics simulations, biochemical assays, and myofibril mechanics to reveal that the G256E myosin variant slows ADP release from myosin during contraction, contributing to pathological hypercontractility.
- Kerry Y. Kao
- Matthew Carter Childers
- Michael Regnier
