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Article

Alterations at the cross-bridge level are associated with a paradoxical gain of muscle function in vivo in a mouse model of nemaline myopathy.

PloS one - 1 Jan 2014

Gineste Charlotte, Ottenheijm Coen, Le Fur Yann, Banzet Sébastien, Pecchi Emilie, Vilmen Christophe, Cozzone Patrick J, Koulmann Nathalie, Hardeman Edna C, Bendahan David, Gondin Julien

Abstract excerpt

Nemaline myopathy is the most common disease entity among non-dystrophic skeletal muscle congenital diseases. The first disease causing mutation (Met9Arg) was identified in the gene encoding α-tropomyosin slow gene (TPM3). Considering the conflicting findings of the previous studies on the transgenic (Tg) mice carrying the TPM3Met9Arg mutation, we investigated carefully the effect of the Met9Arg mutation in 8-9...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Muscle, Skeletal

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Share to Myopathies, Nemaline

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Source

Open in PubMed Open full text

Identifiers

PMID: 25268244
DOI: 10.1371/journal.pone.0109066
PMCID: PMC4182639

Genes

TPM3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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Alterations at the cross-bridge level are associated with a paradoxical gain of muscle function in vivo in a mouse model of nemaline myopathy.PMID 25268244Read ↗

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