L. A. Leinwand

A Conserved Mechanism of Cardiac Hypertrophy Regression through FoxO1

This study identifies FoxO1-dependent autophagy as a conserved mechanism for regression of physiological cardiac hypertrophy across species.

Divergent Molecular Phenotypes in Point Mutations at the Same Residue in Beta-Myosin Heavy Chain Lead to Distinct Cardiomyopathies

This study shows that two point mutations at the same residue in beta-myosin heavy chain cause distinct cardiomyopathies through different molecular mechanisms.

Homologous mutations in β, embryonic, and perinatal muscle myosins have divergent effects on molecular power generation

This study compares the effects of homologous mutations in three muscle myosin isoforms, finding divergent molecular impacts that correlate with disease severity.

Drug specificity and affinity are encoded in the probability of cryptic pocket opening in myosin motor domains

This paper shows that the probability of cryptic pocket opening in myosin motor domains predicts drug specificity and affinity, using molecular dynamics simulations and Markov state models.

Myosin motor domains carrying mutations implicated in early or late onset Hypertrophic Cardiomyopathy have similar properties

The paper analyzes myosin motor domain mutations in Hypertrophic Cardiomyopathy to compare early and late onset mutations, finding no clear functional differences but identifying distinct changes from DCM mutations.

miR-1/206 down-regulates splicing factor Srsf9 to promote myogenesis

This study identifies Srsf9 as a target of miR-1 and miR-206, showing its down-regulation promotes myogenesis by impairing myotube formation and differentiation markers.

Cardiac contraction velocity has evolved to match heart rate with body size through variation in β-cardiac myosin sequence.

The paper identifies amino acid sites in β-cardiac myosin associated with body mass and shows that altering these sites can adjust contraction velocity and ADP release rate.

Cardiac myocytes respond differentially and synergistically to matrix stiffness and topography

This study shows that cardiac myocytes respond differently to matrix stiffness and topography, with synergistic effects on their phenotype, highlighting that alignment alone does not indicate cellular health.

The ATPase cycle of Human Muscle Myosin II Isoforms: Adaptation of a single mechanochemical cycle for different physiological roles.

The paper uses MUSICO to model how cross-bridge cycles of human myosin II isoforms predict muscle fiber contraction characteristics.