The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
TRPC1 binds to caveolin-3 and is regulated by Src kinase – role in Duchenne muscular dystrophy
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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Cites
Dystrophin: the protein product of the Duchenne muscular dystrophy locus
Hoffman, E. P., Brown, R. H., & Kunkel, L. M. (1987) · Cell · doi:10.1016/0092-8674(87)90579-4 · Cited by 4,693
Cited by
Allen, D. G., Whitehead, N. P., & Froehner, S. C. (2016) · Physiological Reviews · doi:10.1152/physrev.00007.2015 · Cited by 426
Self-citationHsp72 preserves muscle function and slows progression of severe muscular dystrophy
Gehrig, S. M., van der Poel, C., Sayer, T. A., Schertzer, J. D., Henstridge, D. C., Church, J. E., Lamon, S., Russell, A. P., Davies, K. E., Febbraio, M. A., et al. (2012) · Nature · doi:10.1038/nature10980 · Cited by 250
Whiteman, I. T., Gervasio, O. L., Cullen, K. M., Guillemin, G. J., Jeong, E. V., Witting, P. K., Antao, S. T., Minamide, L. S., Bamburg, J. R., & Goldsbury, C. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.3531-09.2009 · Cited by 92
Self-citationChung, H. S., Kim, G. E., Holewinski, R. J., Venkatraman, V., Zhu, G., Bedja, D., Kass, D. A., & Van Eyk, J. E. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1712623114 · Cited by 33
Master Regulators of Muscle Atrophy: Role of Costamere Components
Gorza, L., Sorge, M., Seclì, L., & Brancaccio, M. (2021) · Cells · doi:10.3390/cells10010061 · Cited by 31
Metadata
- Authors
- Gervásio, O. L., Whitehead, N. P., Yeung, E. W., Phillips, W. D., & Allen, D. G.
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- 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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- 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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