ArticleThe Journal of cell biology1996
Formation of triads without the dihydropyridine receptor alpha subunits in cell lines from dysgenic skeletal muscle.
Article in The Journal of cell biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 95 citations in OpenAlex.
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- Effects of aging on calcium channels in skeletal muscle.Frontiers in molecular biosciences · 2025Review
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- The Sarcoplasmic Reticulum of Skeletal Muscle Cells: A Labyrinth of Membrane Contact Sites.Biomolecules · 2022Review
- Structures of the junctophilin/voltage-gated calcium channel interface reveal hot spot for cardiomyopathy mutations.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Ion-pair interactions between voltage-sensing domain IV and pore domain I regulate CaBiophysical journal · 2021Article
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- Skeletal muscle CaPflugers Archiv : European journal of physiology · 2020Review
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- Duplex signaling by CaM and Stac3 enhances CaThe Journal of general physiology · 2018Article
- Physical interaction of junctophilin and the CaProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Role of putative voltage-sensor countercharge D4 in regulating gating properties of CaChannels (Austin, Tex.) · 2018Article
- Structural insights into binding of STAC proteins to voltage-gated calcium channels.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- STAC3 stably interacts through its C1 domain with CaScientific reports · 2017Article
- The mammalian skeletal muscle DHPR has larger CaCell calcium · 2017Article
- Two distinct voltage-sensing domains control voltage sensitivity and kinetics of current activation in CaV1.1 calcium channels.The Journal of general physiology · 2016Article
- Physiological and pharmacological modulation of the embryonic skeletal muscle calcium channel splice variant CaV1.1e.Biophysical journal · 2015Article
- Towards a Unified Theory of Calmodulin Regulation (Calmodulation) of Voltage-Gated Calcium and Sodium Channels.Current molecular pharmacology · 2015Review
- N-WASP is required for Amphiphysin-2/BIN1-dependent nuclear positioning and triad organization in skeletal muscle and is involved in the pathophysiology of centronuclear myopathy.EMBO molecular medicine · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Muscular dysgenesis (mdg/mdg), a mutation of the skeletal muscle dihydropyridine receptor (DHPR) alpha 1 subunit, has served as a model to study the functions of the DHPR in excitation-contraction coupling and its role in triad formation. We have investigated the question of whether the lack of the DHPR in dysgenic skeletal muscle results in a failure of triad formation, using cell lines (GLT and NLT) derived from dysgenic (mdg/mdg) and normal (+/+) muscle, respectively. The lines were generated by transfection of myoblasts with a plasmid encoding a Large T antigen. Both cell lines express muscle-specific proteins and begin organization of sarcomeres as demonstrated by immunocytochemistry. Similar to primary cultures, dysgenic (GLT) myoblasts show a higher incidence of cell fusion than their normal counterparts (NLT). NLT myotubes develop spontaneous contractile activity, and fluorescent Ca2+ recordings show Ca2+ release in response to depolarization. In contrast, GLTs show neither spontaneous nor depolarization-induced Ca2+ transients, but do release Ca2+ from the sarcoplasmic reticulum (SR) in response to caffeine. Despite normal transverse tubule (T-tubule) formation, GLT myotubes lack the alpha 1 subunit of the skeletal muscle DHPR, and the alpha 2 subunit is mistargeted. Nevertheless, the ryanodine receptor (RyR) frequently develops its normal, clustered organization in the absence of both DHPR alpha subunits in the T-tubules. In EM, these RyR clusters correspond to T-tubule/SR junctions with regularly spaced feet. These findings provide conclusive evidence that interactions between the DHPR and RyR are not involved in the formation of triad junctions or in the normal organization of the RyR in the junctional SR.
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