ArticleChannels (Austin, Tex.)
The cardiac alpha(1C) subunit can support excitation-triggered Ca2+ entry in dysgenic and dyspedic myotubes.
Article in Channels (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Into the spotlight: RGK proteins in skeletal muscle.Cell calcium · 2021Review
- Preclinical model systems of ryanodine receptor 1-related myopathies and malignant hyperthermia: a comprehensive scoping review of works published 1990-2019.Orphanet journal of rare diseases · 2020Article
- A skeletal muscle L-type CaThe Journal of biological chemistry · 2018Article
- RGK protein-mediated impairment of slow depolarization- dependent Ca2+ entry into developing myotubes.Channels (Austin, Tex.) · 2014Article
- Ca(V)1.1: The atypical prototypical voltage-gated Ca²⁺ channel.Biochimica et biophysica acta · 2013Review
- Dantrolene-induced inhibition of skeletal L-type Ca2+ current requires RyR1 expression.BioMed research international · 2013Article
- Modification of STIM1 by O-linked N-acetylglucosamine (O-GlcNAc) attenuates store-operated calcium entry in neonatal cardiomyocytes.The Journal of biological chemistry · 2012Article
- Divergent biophysical properties, gating mechanisms, and possible functions of the two skeletal muscle Ca(V)1.1 calcium channel splice variants.Journal of muscle research and cell motility · 2011Article
- Reciprocal dihydropyridine and ryanodine receptor interactions in skeletal muscle activation.Journal of muscle research and cell motility · 2011Review
- The role of store-operated calcium influx in skeletal muscle signaling.Cell calcium · 2011Review
- Functional expression of transgenic 1sDHPR channels in adult mammalian skeletal muscle fibres.The Journal of physiology · 2011Article
- A malignant hyperthermia-inducing mutation in RYR1 (R163C): alterations in Ca2+ entry, release, and retrograde signaling to the DHPR.The Journal of general physiology · 2010Article
- Properties of Na+ currents conducted by a skeletal muscle L-type Ca2+ channel pore mutant (SkEIIIK).Channels (Austin, Tex.)Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Depolarization-induced entry of divalent ions into skeletal muscle has been attributed to a process termed Excitation-Coupled Ca(2+) Entry (ECCE), which is hypothesized to require the interaction of the ryanodine receptor (RyR1), the L-type Ca(2+) channel (DHPR) and another unidentified cation channel. Thus, ECCE is absent in myotubes lacking either the DHPR (dysgenic) or RyR1 (dyspedic). Furthermore, ECCE, as measured by Mn(2+) quench of Fura-2, is reconstituted by expression of a mutant DHPR alpha(1S) subunit (SkEIIIK) thought to be impermeable to divalent cations. Previously, we showed that the bulk of depolarization-induced Ca(2+) entry could be explained by the skeletal L-type current. Accordingly, one would predict that any Ca(2+) current similar to the endogenous current would restore such entry and that this entry would not require coupling to either the DHPR or RyR1. Here, we show that expression of the cardiac alpha(1C) subunit in either dysgenic or dyspedic myotubes does result in Ca(2+) entry similar to that ascribed to ECCE. We also demonstrate that, when potentiated by strong depolarization and Bay K 8644, SkEIIIK supports entry of Mn(2+). These results strongly support the idea that the L-type channel is the major route of Ca(2+) entry in response to repetitive or prolonged depolarization of skeletal muscle.
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