Desensitization of the Cardiac Troponin Complex by TnI Phosphorylation and Epigallocatechin-3-Gallate.

ABSTRACT: Cardiac contractility is regulated by the Ca²⁺ sensitivity of thin filaments, largely controlled by troponin I (TnI). Phosphorylation of TnI at Ser23/24 and the green tea catechin (-)-epigallocatechin-3-gallate (EGCG) both reduce thin filament Ca²⁺ responsiveness, yet the underlying structural mechanisms remain incompletely defined. Here, we integrate in vitro motility assays with AlphaFold 3 modeling and molecular dynamics (MD) simulations to characterize the effects of TnI phosphorylation and EGCG on the troponin complex. Motility assays using reconstituted thin filaments showed that TnI Ser23/24 phosphorylation reduced maximum sliding velocity (V _max) by -49 ± 7% and shifted pCa₅₀ by -3 ± 2%. EGCG caused a greater decrease in V <

SUBMITTER: Tigro H 

PROVIDER: S-EPMC12809369 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature