Shirley Sutton

Biophysical properties of human β-cardiac myosin with converter mutations that cause hypertrophic cardiomyopathy

The paper analyzes biophysical properties of human β-cardiac myosin with HCM-causing converter domain mutations, finding minimal changes or slightly hypo-contractile profiles, contrasting with clinical hyper-contractility.

Beyond the myosin mesa: a potential unifying hypothesis on the underlying molecular basis of hyper-contractility caused by a majority of hypertrophic cardiomyopathy mutations

This paper proposes a unifying hypothesis that hypertrophic cardiomyopathy mutations increase functionally accessible myosin heads in the sarcomere, leading to hyper-contractility.