Kathleen M. Ruppel

The E525K β-Myosin Mutation Causes Hypocontractility in Cardiomyocytes Without Altering Crossbridge Cycling

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

The hypertrophic cardiomyopathy mutation G768R makes cardiac myosin a high duty ratio motor

This paper studies the G768R mutation in cardiac myosin, showing it increases the duty ratio to >60%, leading to hypercontractility and impaired relaxation.

The G256E HCM mutation prolongs relaxation via altered nucleotide handling

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

A FRET assay to quantitate levels of the human β-cardiac myosin interacting heads motif based on its near-atomic resolution structure

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.

Multi-scale models reveal hypertrophic cardiomyopathy MYH7 G256E mutation drives hypercontractility and elevated mitochondrial respiration

This study investigates the effects of the MYH7 G256E mutation on myosin function across multiple scales, finding increased hypercontractility and mitochondrial respiration.