ArticleSkeletal muscle2015
Ca(2+) permeation and/or binding to CaV1.1 fine-tunes skeletal muscle Ca(2+) signaling to sustain muscle function.
Article in Skeletal muscle, 2015. 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.
- Complement C3 inhibition restores myasthenia gravis AChR antibody-mediated muscle pathophysiology.EBioMedicine · 2026Article
- Direct Effects of Capsaicin on Voltage-Dependent Calcium Channels of Mammalian Skeletal Muscle.Biomolecules · 2026Article
- A novel, patient-derived RyR1 mutation impairs muscle function and calcium homeostasis in mice.The Journal of general physiology · 2024Article
- Two zebrafish cacna1s loss-of-function variants provide models of mild and severe CACNA1S-related myopathy.Human molecular genetics · 2024Article
- Advances in CaChannels (Austin, Tex.) · 2023Review
- Article
- Pannexin-1 and CaV1.1 show reciprocal interaction during excitation-contraction and excitation-transcription coupling in skeletal muscle.The Journal of general physiology · 2021Article
- Voltage sensor movements of CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Into the spotlight: RGK proteins in skeletal muscle.Cell calcium · 2021Review
- Article
- Sarcolipin Exhibits Abundant RNA Transcription and Minimal Protein Expression in Horse Gluteal Muscle.Veterinary sciences · 2020Article
- Skeletal muscle CaPflugers Archiv : European journal of physiology · 2020Review
- Equivalent L-type channel (CaBiochemical and biophysical research communications · 2020Article
- Zebrafish as a Model System for the Study of Severe CaFrontiers in molecular neuroscience · 2019Review
- Fibroblast growth factor 23 does not directly influence skeletal muscle cell proliferation and differentiation or ex vivo muscle contractility.American journal of physiology. Endocrinology and metabolism · 2018Article
- Oxidative stress-induced dysregulation of excitation-contraction coupling contributes to muscle weakness.Journal of cachexia, sarcopenia and muscle · 2018Article
- When muscle CaThe Journal of physiology · 2018Review
- A skeletal muscle L-type CaThe Journal of biological chemistry · 2018Article
- Molecular Basis for Exercise-Induced Fatigue: The Importance of Strictly Controlled Cellular CaCold Spring Harbor perspectives in medicine · 2018Review
- The CaNature communications · 2017Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
backgroundCa(2+) influx through CaV1.1 is not required for skeletal muscle excitation-contraction coupling, but whether Ca(2+) permeation through CaV1.1 during sustained muscle activity plays a functional role in mammalian skeletal muscle has not been assessed.
methodsWe generated a mouse with a Ca(2+) binding and/or permeation defect in the voltage-dependent Ca(2+) channel, CaV1.1, and used Ca(2+) imaging, western blotting, immunohistochemistry, proximity ligation assays, SUnSET analysis of protein synthesis, and Ca(2+) imaging techniques to define pathways modulated by Ca(2+) binding and/or permeation of CaV1.1. We also assessed fiber type distributions, cross-sectional area, and force frequency and fatigue in isolated muscles.
resultsUsing mice with a pore mutation in CaV1.1 required for Ca(2+) binding and/or permeation (E1014K, EK), we demonstrate that CaV1.1 opening is coupled to CaMKII activation and refilling of sarcoplasmic reticulum Ca(2+) stores during sustained activity. Decreases in these Ca(2+)-dependent enzyme activities alter downstream signaling pathways (Ras/Erk/mTORC1) that lead to decreased muscle protein synthesis. The physiological consequences of the permeation and/or Ca(2+) binding defect in CaV1.1 are increased fatigue, decreased fiber size, and increased Type IIb fibers.
conclusionsWhile not essential for excitation-contraction coupling, Ca(2+) binding and/or permeation via the CaV1.1 pore plays an important modulatory role in muscle performance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.