ArticleBMC physiology2001
Modulation of L-type Ca2+ current but not activation of Ca2+ release by the gamma1 subunit of the dihydropyridine receptor of skeletal muscle.
Article in BMC physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- 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
- Stac3 has a direct role in skeletal muscle-type excitation-contraction coupling that is disrupted by a myopathy-causing mutation.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- 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
- Robust L-type calcium current expression following heterozygous knockout of the Cav1.2 gene in adult mouse heart.The Journal of physiology · 2011Article
- Triadin deletion induces impaired skeletal muscle function.The Journal of biological chemistry · 2009Article
- Absence of regulation of the T-type calcium current by Cav1.1, beta1a and gamma1 dihydropyridine receptor subunits in skeletal muscle cells.Pflugers Archiv : European journal of physiology · 2008Article
- gamma1-dependent down-regulation of recombinant voltage-gated Ca2+ channels.Cellular and molecular neurobiology · 2007Article
- A functional AMPA receptor-calcium channel complex in the postsynaptic membrane.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Functional roles of the gamma subunit of the skeletal muscle DHP-receptor.Journal of muscle research and cell motility · 2006Review
- Altered inactivation of Ca2+ current and Ca2+ release in mouse muscle fibers deficient in the DHP receptor gamma1 subunit.The Journal of general physiology · 2004Article
- Membrane cholesterol modulates dihydropyridine receptor function in mice fetal skeletal muscle cells.The Journal of physiology · 2004Article
- Ca2+-dependent excitation-contraction coupling triggered by the heterologous cardiac/brain DHPR beta2a-subunit in skeletal myotubes.Biophysical journal · 2003Article
- Article
- The novel product of a five-exon stargazin-related gene abolishes Ca(V)2.2 calcium channel expression.The EMBO journal · 2002Article
- Skeletal muscle L-type Ca(2+) current modulation in gamma1-deficient and wildtype murine myotubes by the gamma1 subunit and cAMP.The Journal of physiology · 2002Article
- Functional analysis of a frame-shift mutant of the dihydropyridine receptor pore subunit (alpha1S) expressing two complementary protein fragments.BMC physiology · 2001Article
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundThe multisubunit (alpha1S,alpha2-delta, beta1a and gamma1) skeletal muscle dihydropyridine receptor (DHPR) transduces membrane depolarization into release of Ca2+ from the sarcoplasmic reticulum (SR) and also acts as an L-type Ca2+ channel. To more fully investigate the function of the gamma1 subunit in these two processes, we produced mice lacking this subunit by gene targeting.
resultsMice lacking the DHPR gamma1 subunit (gamma1 null) survive to adulthood, are fertile and have no obvious gross phenotypic abnormalities. The gamma1 subunit is expressed at approximately half the normal level in heterozygous mice (gamma1 het). The density of the L-type Ca2+ current in gamma1 null and gamma1 het myotubes was higher than in controls. Inactivation of the Ca2+ current produced by a long depolarization was slower and incomplete in gamma1 null and gamma1 het myotubes, and was shifted to a more positive potential than in controls. However, the half-activation potential of intramembrane charge movements was not shifted, and the maximum density of the total charge was unchanged. Also, no shift was observed in the voltage-dependence of Ca2+ transients. gamma1 null and gamma1 het myotubes had the same peak Ca2+ amplitude vs. voltage relationship as control myotubes.
conclusionsThe L-type Ca2+ channel function, but not the SR Ca2+ release triggering function of the skeletal muscle dihydropyridine receptor, is modulated by the gamma1 subunit.
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