ArticleProceedings of the National Academy of Sciences of the United States of America1995
Abnormal junctions between surface membrane and sarcoplasmic reticulum in skeletal muscle with a mutation targeted to the ryanodine receptor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 130 citations in OpenAlex.
- Structural insights into transmembrane helix S0 facilitated RyR1 channel gating by CaNature communications · 2025Article
- From function to structure: how myofibrillogenesis influences the transverse-axial tubular system development and its peculiarities.Frontiers in physiology · 2025Review
- Endoplasmic Reticulum-Plasma Membrane Junctions as Sites of Depolarization-Induced CaAnnual review of physiology · 2023Review
- The distal C terminus of the dihydropyridine receptor βProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Ablation of Calsequestrin-1, CaFrontiers in physiology · 2022Review
- Common Pathogenic Mechanisms in Centronuclear and Myotubular Myopathies and Latest Treatment Advances.International journal of molecular sciences · 2021Review
- Neuronal junctophilins recruit specific CaeLife · 2021Article
- Physiological and Pathological Relevance of Selective and Nonselective CaAdvances in experimental medicine and biology · 2021Article
- From Mice to Humans: An Overview of the Potentials and Limitations of Current Transgenic Mouse Models of Major Muscular Dystrophies and Congenital Myopathies.International journal of molecular sciences · 2020Review
- CaCells · 2019Review
- Cored in the act: the use of models to understand core myopathies.Disease models & mechanisms · 2019Review
- Mouse model of severe recessive RYR1-related myopathy.Human molecular genetics · 2019Article
- Severe Neonatal RYR1 Myopathy With Pathological Features of Congenital Muscular Dystrophy.Journal of neuropathology and experimental neurology · 2019Article
- Calcium-induced release of calcium in muscle: 50 years of work and the emerging consensus.The Journal of general physiology · 2018Review
- The relationship between form and function throughout the history of excitation-contraction coupling.The Journal of general physiology · 2018Review
- The structural basis of ryanodine receptor ion channel function.The Journal of general physiology · 2017Review
- ER-plasma membrane junctions: Why and how do we study them?Biochimica et biophysica acta. Molecular cell research · 2017Review
- Physiology and pathophysiology of excitation-contraction coupling: the functional role of ryanodine receptor.Journal of muscle research and cell motility · 2017Review
- Structural and functional properties of ryanodine receptor type 3 in zebrafish tail muscle.The Journal of general physiology · 2015Article
- The disorders of the calcium release unit of skeletal muscles: what have we learned from mouse models?Journal of muscle research and cell motility · 2015Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Junctions that mediate excitation-contraction (e-c) coupling are formed between the sarcoplasmic reticulum (SR) and either the surface membrane or the transverse (T) tubules in normal skeletal muscle. Two structural components of the junctions, the feet of the SR and the tetrads of T tubules, have been identified respectively as ryanodine receptors (RyRs, or SR calcium-release channels), and as groups of four dihydropyridine receptors (DHPRs, or voltage sensors of e-c coupling). A targeted mutation (skrrm1) of the gene for skeletal muscle RyRs in mice results in the absence of e-c coupling in homozygous offspring of transgenic parents. The mutant gene is expected to produce no functional RyRs, and we have named the mutant mice "dyspedic" because they lack feet--the cytoplasmic domain of RyRs anchored in the SR membrane. We have examined the development of junctions in skeletal muscle fibers from normal and dyspedic embryos. Surprisingly, despite the absence of RyRs, junctions are formed in dyspedic myotubes, but the junctional gap between the SR and T tubule is narrow, presumably because the feet are missing. Tetrads are also absent from these junctions. The results confirm the identity of RyRs and feet and a major role for RyRs and tetrads in e-c coupling. Since junctions form in the absence of feet and tetrads, coupling of SR to surface membrane and T tubules appears to be mediated by additional proteins, distinct from either RyRs or DHPRs.
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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.