Together, we used single molecule techniques, in vitro reconstitution assays, and molecular dynamics simulations to demonstrate that this linker region is intrinsically disordered and dynamic in the context of isolated troponin and the fully-regulated thin filament. We also demonstrate how rigorous tools developed by the intrinsically disordered protein field can provide new insights into the structural mechanisms underlying human cardiomyopathy mutations. Congratulations to all of our co-authors!
The paper can be found here.