Glutamate 139 of tropomyosin is critical for cardiac thin filament blocked-state stabilization.

ABSTRACT: The cardiac thin filament proteins troponin and tropomyosin control actomyosin formation and thus cardiac contractility. Calcium binding to troponin changes tropomyosin position along the thin filament, allowing myosin head binding to actin required for heart muscle contraction. The thin filament regulatory proteins are hot spots for genetic mutations causing heart muscle dysfunction. While much of the thin filament structure has been characterized, critical regions of troponin and tropomyosin involved in triggering conformational changes remain unresolved. A poorly resolved region, helix-4 (H₄) of troponin I, is thought to stabilize tropomyosin in a position on actin that blocks actomyosin interactions at low calcium concentrations during muscle relaxation. We have proposed tha

SUBMITTER: Barry ME 

PROVIDER: S-EPMC11654406 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature