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TRPC1 binds to caveolin-3 and is regulated by Src kinase – role in Duchenne muscular dystrophy

Gervásio, Othon L., Whitehead, Nicholas P., Yeung, Ella W., Phillips, William D., Allen, David G.·2008·Journal of Cell Science

Abstract

Transient receptor potential canonical 1 (TRPC1), a widely expressed calcium (Ca2+)-permeable channel, is potentially involved in the pathogenesis of Duchenne muscular dystrophy (DMD). Ca2+ influx through stretch-activated channels, possibly formed by TRPC1, induces muscle-cell damage in the mdx mouse, an animal model of DMD. In this study, we showed that TRPC1, caveolin-3 and Src-kinase protein levels are increased in mdx muscle compared with wild type. TRPC1 and caveolin-3 colocalised and co-immunoprecipitated. Direct binding of TRPC1-CFP to caveolin-3–YFP was confirmed in C2 myoblasts by fluorescence energy resonance transfer (FRET). Caveolin-3–YFP targeted TRPC1-CFP to the plasma membrane. Hydrogen peroxide, a reactive oxygen species (ROS), increased Src activity and enhanced Ca2+ influx, but only in C2 myoblasts co-expressing TRPC1 and caveolin-3. In mdx muscle, Tiron, a ROS scavenger, and PP2, a Src inhibitor, reduced stretch-induced Ca2+ entry and increased force recovery. Because ROS production is increased in mdx/DMD, these results suggest that a ROS-Src-TRPC1/caveolin-3 pathway contributes to the pathogenesis of mdx/DMD.

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Metadata

Authors
Gervásio, O. L., Whitehead, N. P., Yeung, E. W., Phillips, W. D., & Allen, D. G.
Venue
Journal of Cell Science
Published
2008-07-01
Volume
121
Issue
13
Pages
2246-2255
ISSN
  • 0021-9533 (ISSN-L)
  • 1477-9137
OpenAlex
W2016923561
Cited by
169
References
1
FWCI
6.33
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: TRPC1 binds to caveolin-3 and is regulated by Src kinase – role in Duchenne muscular dystrophy. https://app.cochat.ai/papers/10.1242/jcs.032003
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Gervásio, O. L., Whitehead, N. P., Yeung, E. W., Phillips, W. D., & Allen, D. G. (2008). TRPC1 binds to caveolin-3 and is regulated by Src kinase – role in Duchenne muscular dystrophy. Journal of Cell Science. https://doi.org/10.1242/jcs.032003

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