ArticleProceedings of the National Academy of Sciences of the United States of America2007
The auxiliary subunit gamma 1 of the skeletal muscle L-type Ca2+ channel is an endogenous Ca2+ antagonist.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Smooth muscle of the lower urinary tract: BK-RyR coupling in physiology and pathophysiology.Journal of muscle research and cell motility · 2025Review
- Structural biology of voltage-gated calcium channels.Channels (Austin, Tex.) · 2024Review
- Advances in CaChannels (Austin, Tex.) · 2023Review
- From α1s splicing to γ1 function: A new twist in subunit modulation of the skeletal muscle L-type Ca2+ channel.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
- Role of High Voltage-Gated CaCells · 2021Review
- Transcriptome analysis of gravitational effects on mouse skeletal muscles under microgravity and artificial 1 g onboard environment.Scientific reports · 2021Article
- Detection of Ca2+ transients near ryanodine receptors by targeting fluorescent Ca2+ sensors to the triad.The Journal of general physiology · 2021Article
- Voltage-Gated Calcium Channels in Nonexcitable Tissues.Annual review of physiology · 2021Review
- Tetraspanin-7 regulation of L-type voltage-dependent calcium channels controls pancreatic β-cell insulin secretion.The Journal of physiology · 2020Article
- Skeletal muscle CaPflugers Archiv : European journal of physiology · 2020Review
- Knockdown of Death-Associated Protein Expression Induces Global Transcriptome Changes in Proliferating and Differentiating Muscle Satellite Cells.Frontiers in physiology · 2020Article
- The calcium channel subunit gamma-4 is regulated by MafA and necessary for pancreatic beta-cell specification.Communications biology · 2019Article
- The CaNature communications · 2017Article
- How and why are calcium currents curtailed in the skeletal muscle voltage-gated calcium channels?The Journal of physiology · 2017Review
- Selective pressure modulation of synaptic voltage-dependent calcium channels-involvement in HPNS mechanism.Journal of cellular and molecular medicine · 2016Article
- Article
- The role of auxiliary subunits for the functional diversity of voltage-gated calcium channels.Journal of cellular physiology · 2015Review
- Physiological and pharmacological modulation of the embryonic skeletal muscle calcium channel splice variant CaV1.1e.Biophysical journal · 2015Article
- Three-dimensional localization of the α and β subunits and of the II-III loop in the skeletal muscle L-type Ca2+ channel.The Journal of biological chemistry · 2012Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca2+ channels play crucial roles in cellular signal transduction and are important targets of pharmacological agents. They are also associated with auxiliary subunits exhibiting functions that are still incompletely resolved. Skeletal muscle L-type Ca2+ channels (dihydropyridine receptors, DHPRs) are specialized for the remote voltage control of type 1 ryanodine receptors (RyR1) to release stored Ca2+. The skeletal muscle-specific gamma subunit of the DHPR (gamma 1) down-modulates availability by altering its steady state voltage dependence. The effect resembles the action of certain Ca2+ antagonistic drugs that are thought to stabilize inactivated states of the DHPR. In the present study we investigated the cross influence of gamma 1 and Ca2+ antagonists by using wild-type (gamma+/+) and gamma 1 knockout (gamma-/-) mice. We studied voltage-dependent gating of both L-type Ca2+ current and Ca2+ release and the allosteric modulation of drug binding. We found that 10 microM diltiazem, a benzothiazepine drug, more than compensated for the reduction in high-affinity binding of the dihydropyridine agent isradipine caused by gamma 1 elimination; 5 muM devapamil [(-)D888], a phenylalkylamine Ca2+ antagonist, approximately reversed the right-shifted voltage dependence of availability and the accelerated recovery kinetics of Ca2+ current and Ca2+ release. Moreover, the presence of gamma 1 altered the effect of D888 on availability and strongly enhanced its impact on recovery kinetics demonstrating that gamma 1 and the drug do not act independently of each other. We propose that the gamma 1 subunit of the DHPR functions as an endogenous Ca2+ antagonist whose task may be to minimize Ca2+ entry and Ca2+ release under stress-induced conditions favoring plasmalemma depolarization.
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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.