ArticleProceedings of the National Academy of Sciences of the United States of America2013
Skeletal muscle-specific T-tubule protein STAC3 mediates voltage-induced Ca2+ release and contractility.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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Who cites it
94 citing papers in PubMed, 134 citations in OpenAlex.
- Article
- Pathogenic CaCommunications biology · 2026Article
- Article
- Article
- LL-37 Inhibits EV71 Infection by Upregulating STAC via the EGFR-ERK Signaling Pathway.Viruses · 2026Article
- STAC3 binding to CaV1.1 II-III loop is nonessential but critically supports skeletal muscle excitation-contraction coupling.JCI insight · 2025Article
- The molecular transition that confers voltage dependence to muscle contraction.Nature communications · 2025Article
- ERG1A KScientific reports · 2025Article
- Inactivation of CaV1 and CaV2 channels.The Journal of general physiology · 2025Review
- Intracellular Membrane Contact Sites in Skeletal Muscle Cells.Membranes · 2025Review
- In situ structural insights into the excitation-contraction coupling mechanism of skeletal muscle.Science advances · 2024Article
- The T-type calcium channelosome.Pflugers Archiv : European journal of physiology · 2024Review
- Advances in CaChannels (Austin, Tex.) · 2023Review
- Mechanical loading is required for initiation of extracellular matrix deposition at the developing murine myotendinous junction.Matrix biology : journal of the International Society for Matrix Biology · 2023Article
- CaHandbook of experimental pharmacology · 2023Article
- NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023Review
- A reconstituted depolarization-induced Ca2+ release platform for validation of skeletal muscle disease mutations and drug discovery.The Journal of general physiology · 2022Article
- Calcium current modulation by the γ1 subunit depends on alternative splicing of CaV1.1.The Journal of general physiology · 2022Article
- Molecular interactions of STAC proteins with skeletal muscle dihydropyridine receptor and excitation-contraction coupling.Protein science : a publication of the Protein Society · 2022Article
- The Sarcoplasmic Reticulum of Skeletal Muscle Cells: A Labyrinth of Membrane Contact Sites.Biomolecules · 2022Review
34 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Excitation-contraction (EC) coupling comprises events in muscle that convert electrical signals to Ca(2+) transients, which then trigger contraction of the sarcomere. Defects in these processes cause a spectrum of muscle diseases. We report that STAC3, a skeletal muscle-specific protein that localizes to T tubules, is essential for coupling membrane depolarization to Ca(2+) release from the sarcoplasmic reticulum (SR). Consequently, homozygous deletion of src homology 3 and cysteine rich domain 3 (Stac3) in mice results in complete paralysis and perinatal lethality with a range of musculoskeletal defects that reflect a blockade of EC coupling. Muscle contractility and Ca(2+) release from the SR of cultured myotubes from Stac3 mutant mice could be restored by application of 4-chloro-m-cresol, a ryanodine receptor agonist, indicating that the sarcomeres, SR Ca(2+) store, and ryanodine receptors are functional in Stac3 mutant skeletal muscle. These findings reveal a previously uncharacterized, but required, component of the EC coupling machinery of skeletal muscle and introduce a candidate for consideration in myopathic disorders.
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