Robert C. Cail

This paper investigates the HCM mutation M493I in β-cardiac myosin, showing it disrupts the super-relaxed state, slows ADP release, and enhances actin attachment and force production, leading to hypercontractility.

This paper identifies a novel epitope (S2Tag) recognized by an antibody that effectively tethers coiled-coil proteins, demonstrating its utility in studying β-cardiac myosin mechanics and disease mutations.

This study investigates the dynamics between the super-relaxed (SRX) and disordered-relaxed (DRX) states of β-cardiac myosin, showing they are in rapid equilibrium and how mutations and inhibitors affect this balance.