Michael J. Greenberg

This study shows that mitophagy removes cytosolic protein aggregates in cardiac myocytes, preventing cardiomyopathy, and that TRAF2 modulation affects this process.

This study models human iron overload cardiomyopathy in vitro using engineered heart tissues, revealing differential effects on cardiomyocytes and fibroblasts and mechanisms of arrhythmogenesis and reduced contractility.

The paper introduces an unbiased proteomic platform for ATE1-based arginylation profiling, identifying 235 unique arginylation sites in human proteomes.

This study investigates danicamtiv's effects on cardiac myosin mechanics and shows it enhances contraction by altering crossbridge kinetics and thin filament activation.

This study shows that the ACTA1 R256H mutation disrupts actin structure and function in cardiomyocytes, leading to reduced contractility and a likely causative role in dilated cardiomyopathy.

This paper investigates the structural dynamics of the intrinsically disordered troponin-T linker region using single-molecule FRET, molecular dynamics simulations, and functional assays, showing its dynamic behavior and how a mutation affects intermolecular interactions.

This study shows that loss of p300 and CBP in skeletal muscle causes severe contractile dysfunction, but mitochondrial function and cross-bridge cycling are not the primary causes.

This study connects genotype, phenotype, and drug response in dilated cardiomyopathy using molecular mechanism-based computational and experimental approaches for a troponin T mutation.

This study uses zebrafish to model TPM2 variants associated with musculoskeletal disorders, finding correlations between variant severity and clinical outcomes.