Weikang Ma

This paper uses polarized second-harmonic generation microscopy to analyze myosin states in hypertrophic cardiomyopathy, showing increased ON state fraction in mutated tissue.

This study compares the structural and functional properties of porcine left atrial and ventricular myosin filaments, revealing distinct calcium-dependent regulatory mechanisms between the two chambers.

This study shows that different MyBP-C paralogs have similar effects on cross-bridge cycling but distinct responses to rapid stretch, with MyBP-C limiting strain-induced detachment in fast-twitch muscles.

This study investigates the R403Q mutation in beta-myosin heavy chain using porcine and human stem cell models, revealing altered contractile properties and mechanisms of hypercontractility and impaired relaxation.

This study shows that DSG2 deficiency causes cardiac dysfunction by impairing Z-disc and intercalated disc mechanotransduction, leading to structural and functional cardiac defects.

This study examines how mavacamten affects skeletal muscle structure by reducing ON-state myosin heads and shortening thin filament length, similar to its effects in cardiac muscle.

The paper uses an atomic model of the human cardiac thick filament to compute contributions of different components to X-ray diffraction patterns, confirming some interpretations and contradicting others.

This paper shows Aficamten inhibits cardiac myosin ATPase without changing thick filament structure, unlike Mavacamten, leading to similar force reduction but different kinetic effects.

This study investigates the effects of MyBP-C knockout in skeletal muscle, finding altered length-dependent activation and myofilament structure, with implications for MyBP-C-related diseases.

The paper investigates how titin-based forces affect cardiac myofilament structures under stretch, supporting the Frank-Starling mechanism.

This study decouples structural OFF/ON states from biochemical SRX/DRX states in myosin using X-ray diffraction and ATP assays in porcine myocardium.

This study identifies sMyBP-C's critical role in skeletal muscle development and function using gene-edited mouse models, showing its necessity for prenatal and postnatal muscle growth and structural integrity.

This study shows that MyBP-CC1C7 domains form C-links and stabilize myosin OFF states, affecting crossbridge kinetics and sarcomere function.