Abstract
We have solved high-resolution structures of the human cardiac actin-myosin complex and correlated our findings with kinetics data of the actomyosin ATPase. Our long-range goal is to compare the behavior of wild-type and mutant sarcomeric proteins on assembled thin filament complexes using human cardiac-specific proteins. Furthermore, we aim to dock small compounds into pockets associated with the thin filament-myosin interface as a means of mitigating effects of mutations. To date, human β-cardiac myosin subfragment 1 (M2β-S1, amino acids 1-843) was expressed with C-terminal Avi and FLAG tags in C2C12 cells.
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