ArticleDevelopment (Cambridge, England)2016
Restricting calcium currents is required for correct fiber type specification in skeletal muscle.
Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
31 citing papers in PubMed, 43 citations in OpenAlex.
- Elimination of myotonia improves myopathy in a muscleblind-like knockout model of myotonic dystrophy.Nature communications · 2026Article
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- Direct Effects of Capsaicin on Voltage-Dependent Calcium Channels of Mammalian Skeletal Muscle.Biomolecules · 2026Article
- CaNature communications · 2024Article
- Two zebrafish cacna1s loss-of-function variants provide models of mild and severe CACNA1S-related myopathy.Human molecular genetics · 2024Article
- Verapamil mitigates chloride and calcium bi-channelopathy in a myotonic dystrophy mouse model.The Journal of clinical investigation · 2024Article
- Case report: Dihydropyridine receptor (Frontiers in neurology · 2024Article
- Curcumin Administration Improves Force ofAntioxidants (Basel, Switzerland) · 2023Article
- CaHandbook of experimental pharmacology · 2023Article
- Disrupted T-tubular network accounts for asynchronous calcium release in MTM1-deficient skeletal muscle.The Journal of physiology · 2023Article
- Calcium current modulation by the γ1 subunit depends on alternative splicing of CaV1.1.The Journal of general physiology · 2022Article
- Carotenoid transporter CD36 expression depends on hypoxia-inducible factor-1α in mouse soleus muscles.Journal of clinical biochemistry and nutrition · 2022Article
- Article
- RNA Targeting in Inherited Neuromuscular Disorders: Novel Therapeutic Strategies to Counteract Mis-Splicing.Cells · 2021Review
- Article
- Comprehensive analysis and establishment of a prediction model of alternative splicing events reveal the prognostic predictor and immune microenvironment signatures in triple negative breast cancer.Journal of translational medicine · 2020Article
- Skeletal muscle CaPflugers Archiv : European journal of physiology · 2020Review
- Equivalent L-type channel (CaBiochemical and biophysical research communications · 2020Article
- Postsynaptic CaScientific reports · 2019Article
- Correcting the R165K substitution in the first voltage-sensor of CaChannels (Austin, Tex.) · 2019Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Skeletal muscle excitation-contraction (EC) coupling is independent of calcium influx. In fact, alternative splicing of the voltage-gated calcium channel CaV1.1 actively suppresses calcium currents in mature muscle. Whether this is necessary for normal development and function of muscle is not known. However, splicing defects that cause aberrant expression of the calcium-conducting developmental CaV1.1e splice variant correlate with muscle weakness in myotonic dystrophy. Here, we deleted CaV1.1 (Cacna1s) exon 29 in mice. These mice displayed normal overall motor performance, although grip force and voluntary running were reduced. Continued expression of the developmental CaV1.1e splice variant in adult mice caused increased calcium influx during EC coupling, altered calcium homeostasis, and spontaneous calcium sparklets in isolated muscle fibers. Contractile force was reduced and endurance enhanced. Key regulators of fiber type specification were dysregulated and the fiber type composition was shifted toward slower fibers. However, oxidative enzyme activity and mitochondrial content declined. These findings indicate that limiting calcium influx during skeletal muscle EC coupling is important for the secondary function of the calcium signal in the activity-dependent regulation of fiber type composition and to prevent muscle disease.
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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 OpenQuestion graph.