ArticleThe Journal of biological chemistry2009
Regulation of TRPC1 and TRPC4 cation channels requires an alpha1-syntrophin-dependent complex in skeletal mouse myotubes.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 82 citations in OpenAlex.
- Effects of aging on calcium channels in skeletal muscle.Frontiers in molecular biosciences · 2025Review
- Ion Channels of the Sarcolemma and Intracellular Organelles in Duchenne Muscular Dystrophy: A Role in the Dysregulation of Ion Homeostasis and a Possible Target for Therapy.International journal of molecular sciences · 2023Review
- The SOCE Machinery: An Unbalanced Knowledge between Left and Right Ventricular Pathophysiology.Cells · 2022Review
- Evaluation of the dystrophin carboxy-terminal domain for micro-dystrophin gene therapy in cardiac and skeletal muscles in the DMDGene therapy · 2022Article
- Complexity of skeletal muscle degeneration: multi-systems pathophysiology and organ crosstalk in dystrophinopathy.Pflugers Archiv : European journal of physiology · 2021Review
- Role of Store-Operated CaBiomolecules · 2021Review
- Review
- Distribution and Assembly of TRP Ion Channels.Advances in experimental medicine and biology · 2021Article
- Abnormal Calcium Handling in Duchenne Muscular Dystrophy: Mechanisms and Potential Therapies.Frontiers in physiology · 2021Review
- Article
- TRPCs: Influential Mediators in Skeletal Muscle.Cells · 2020Review
- Calcium Channels in Adult Brain Neural Stem Cells and in Glioblastoma Stem Cells.Frontiers in cellular neuroscience · 2020Review
- Article
- Syntrophins entangled in cytoskeletal meshwork: Helping to hold it all together.Cell proliferation · 2019Review
- Biochemical and Functional Interplay Between Ion Channels and the Components of the Dystrophin-Associated Glycoprotein Complex.The Journal of membrane biology · 2018Review
- Article
- The Complex Role of Store Operated Calcium Entry Pathways and Related Proteins in the Function of Cardiac, Skeletal and Vascular Smooth Muscle Cells.Frontiers in physiology · 2018Review
- A focus on extracellular CaExperimental & molecular medicine · 2017Review
- Calcium Channels in Vascular Smooth Muscle.Advances in pharmacology (San Diego, Calif.) · 2017Review
- The involvement of transient receptor potential canonical type 1 in skeletal muscle regrowth after unloading-induced atrophy.The Journal of physiology · 2016Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The dystrophin-associated protein complex (DAPC) is essential for skeletal muscle, and the lack of dystrophin in Duchenne muscular dystrophy results in a reduction of DAPC components such as syntrophins and in fiber necrosis. By anchoring various molecules, the syntrophins may confer a role in cell signaling to the DAPC. Calcium disorders and abnormally elevated cation influx in dystrophic muscle cells have suggested that the DAPC regulates some sarcolemmal cationic channels. We demonstrated previously that mini-dystrophin and alpha1-syntrophin restore normal cation entry in dystrophin-deficient myotubes and that sarcolemmal TRPC1 channels associate with dystrophin and the bound PDZ domain of alpha1-syntrophin. This study shows that small interfering RNA (siRNA) silencing of alpha1-syntrophin dysregulated cation influx in myotubes. Moreover, deletion of the PDZ-containing domain prevented restoration of normal cation entry by alpha1-syntrophin transfection in dystrophin-deficient myotubes. TRPC1 and TRPC4 channels are expressed at the sarcolemma of muscle cells; forced expression or siRNA silencing showed that cation influx regulated by alpha1-syntrophin is supported by TRPC1 and TRPC4. A molecular association was found between TRPC1 and TRPC4 channels and the alpha1-syntrophin-dystrophin complex. TRPC1 and TRPC4 channels may form sarcolemmal channels anchored to the DAPC, and alpha1-syntrophin is necessary to maintain the normal regulation of TRPC-supported cation entry in skeletal muscle. Cation channels with DAPC form a signaling complex that modulates cation entry and may be crucial for normal calcium homeostasis in skeletal muscles.
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Registered trials
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