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Article

Facilitated cross-bridge interactions with thin filaments by familial hypertrophic cardiomyopathy mutations in α-tropomyosin.

Journal of biomedicine & biotechnology - 1 Jan 2011

Wang Fang, Brunet Nicolas M, Grubich Justin R, Bienkiewicz Ewa A, Asbury Thomas M, Compton Lisa A, Mihajlović Goran, Miller Victor F, Chase P Bryant

Abstract excerpt

Familial hypertrophic cardiomyopathy (FHC) is a disease of cardiac sarcomeres. To identify molecular mechanisms underlying FHC pathology, functional and structural differences in three FHC-related mutations in recombinant α-Tm (V95A, D175N, and E180G) were characterized using both conventional and modified in vitro motility assays and circular dichroism spectroscopy. Mutant Tm's exhibited reduced α-helical...

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Identifiers

PMID: 22187526
DOI: 10.1155/2011/435271
PMCID: PMC3237018

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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