Tail length and E525K dilated cardiomyopathy mutant alter human β-cardiac myosin super-relaxed state.

ABSTRACT: Dilated cardiomyopathy (DCM) is a condition characterized by impaired cardiac function, due to myocardial hypo-contractility, and is associated with point mutations in β-cardiac myosin, the molecular motor that powers cardiac contraction. Myocardial function can be modulated through sequestration of myosin motors into an auto-inhibited "super-relaxed" state (SRX), which may be further stabilized by a structural state known as the "interacting heads motif" (IHM). Here, we sought to determine whether hypo-contractility of DCM myocardium results from reduced function of individual myosin molecules or from decreased myosin availability to interact with actin due to increased IHM/SRX stabilization. We used an established DCM myosin mutation, E525K, and characterized the biochemical and mechanic

SUBMITTER: Duno-Miranda S 

PROVIDER: S-EPMC11074782 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature