Theresia Kraft

The paper uses single-molecule techniques to reveal two distinct myosin cycles with different kinetics and stroke sizes affected by mavacamten and omecamtiv mecarbil.

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

This study shows that modGLA mRNA therapy reverses Fabry disease phenotypes in human iPSC-derived cardiomyocytes by restoring enzyme activity and normalizing molecular alterations.

The paper identifies MYOM2 as a candidate gene for hypertrophic cardiomyopathy and Tetralogy of Fallot and shows its functional role in heart development through Drosophila models.