ArticleThe Journal of physiology2014
Utrophin regulates modal gating of mechanosensitive ion channels in dystrophic skeletal muscle.
Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Magnetic Mitohormesis as a Potential Non-Invasive Restorative Therapy for X-Linked Muscular Dystrophies.International journal of molecular sciences · 2026Review
- Upregulation of utrophin improves the phenotype of Duchenne muscular dystrophy hiPSC-derived CMs.Molecular therapy. Nucleic acids · 2024Article
- Multi-omics analysis of sarcospan overexpression in mdx skeletal muscle reveals compensatory remodeling of cytoskeleton-matrix interactions that promote mechanotransduction pathways.Skeletal muscle · 2023Article
- Ambient and supplemental magnetic fields promote myogenesisFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2017Article
- Second-generation compound for the modulation of utrophin in the therapy of DMD.Human molecular genetics · 2015Article
- Disease course in mdx:utrophin+/- mice: comparison of three mouse models of Duchenne muscular dystrophy.Physiological reports · 2015Article
- Utrophin suppresses low frequency oscillations and coupled gating of mechanosensitive ion channels in dystrophic skeletal muscle.Channels (Austin, Tex.) · 2015Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dystrophin is a large, submembrane cytoskeletal protein, absence of which causes Duchenne muscular dystrophy. Utrophin is a dystrophin homologue found in both muscle and brain whose physiological function is unknown. Recordings of single-channel activity were made from membrane patches on skeletal muscle from mdx, mdx/utrn(+/-) heterozygotes and mdx/utrn(-/-) double knockout mice to investigate the role of these cytoskeletal proteins in mechanosensitive (MS) channel gating. We find complex, gene dose-dependent effects of utrophin depletion in dystrophin-deficient mdx muscle: (1) increased MS channel open probability, (2) a shift of MS channel gating to larger pressures, (3) appearance of modal gating of MS channels and small conductance channels and (4) expression of large conductance MS channels. We suggest a physical model in which utrophin acts as a scaffolding protein that stabilizes lipid microdomains and clusters MS channel subunits. Depletion of utrophin disrupts domain composition in a manner that favours open channel area expansion, as well as allowing diffusion and aggregation of additional MS channel subunits.
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