Michael Regnier

The paper re-examines the SRX state in myosin using mant-ATP displacement assays and finds no evidence of the SRX state in isolated myosin but detects two components in myofibrils, suggesting distinct myosin populations in thick filaments.

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

This study investigates how the E525K mutation in cardiac myosin affects its structure and function by analyzing conformational changes using cryo-EM and MD simulations.

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 examines the long-term effects of mavacamten on sarcomere structure and function in hiPSC-derived cardiomyocytes from HCM patients, finding a biphasic reduction in force and structural remodeling.

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

This study investigates the molecular mechanism of cardiac myosin dysfunction caused by the A57D mutation in MLC1v using single-molecule analysis and computational modeling.

The paper identifies altered microtubule post-translational modifications in hypertrophic cardiomyopathy and shows protein kinase A modulates microtubule repolymerization in patient-derived hiPSC-CMs.

The paper uses molecular dynamics simulations to show how conformational changes in loop 2 of myosin affect actomyosin association strength through electrostatic interactions.

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 investigates how HCM mutations Y115H and E497D disrupt the folded-back state of human beta-cardiac myosin, leading to hypercontractility by destabilizing the OFF-state.

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

This study uses single molecule imaging to analyze how phosphorylation affects myosin activity and cardiac reserve in porcine sarcomeres, identifying distinct kinetic states and their modulation by phosphorylation.

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 shows calcium-activated contractility is not needed for sarcomere formation but is essential for cardiomyocyte maturation and response to mechanical cues, with nanopatterns aiding maturation in non-contractile cells.

This study uses molecular dynamics simulations to investigate how 2-deoxy-ATP modifies the structure and dynamics of myosin in the interacting heads motif state.

This paper introduces a new fluorescent sensor, oROS-HT, for real-time H2O2 monitoring with subcellular resolution and multi-parametric imaging capabilities.

The paper identifies heterozygous missense variants in ACTC1 as the cause of distal arthrogryposis with congenital heart defects in five families.

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