ArticleBiophysical journal2009
A CaV1.1 Ca2+ channel splice variant with high conductance and voltage-sensitivity alters EC coupling in developing skeletal muscle.
Article in Biophysical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed.
- Human lymphatic vessel contractile activity is inhibited in vitro but not in vivo by the calcium channel blocker nifedipine.The Journal of physiology · 2014Trial
- Voltage-sensing domains: structural and functional diversity.European biophysics journal : EBJ · 2026Review
- Elimination of myotonia improves myopathy in a muscleblind-like knockout model of myotonic dystrophy.Nature communications · 2026Article
- Pathogenic CaCommunications biology · 2026Article
- A new approach methodology for studying intrinsic ventricular arrhythmias in Fabry disease.Frontiers in cardiovascular medicine · 2026Article
- Myotonic dystrophy type 1: clinical diversity, molecular insights and therapeutic perspectives.Nature reviews. Neurology · 2025Review
- Voltage-sensor gating charge interactions bimodally regulate voltage dependence and kinetics of calcium channel activation.The Journal of general physiology · 2025Article
- Voltage sensors.Molecular pharmacology · 2025Review
- Effects of aging on calcium channels in skeletal muscle.Frontiers in molecular biosciences · 2025Review
- CaNature communications · 2024Article
- Biallelic variants in SNUPN cause a limb girdle muscular dystrophy with myofibrillar-like features.Brain : a journal of neurology · 2024Article
- The Role of Force Fields and Water Models in Protein Folding and Unfolding Dynamics.Journal of chemical theory and computation · 2024Article
- Verapamil mitigates chloride and calcium bi-channelopathy in a myotonic dystrophy mouse model.The Journal of clinical investigation · 2024Article
- Case report: Dihydropyridine receptor (Frontiers in neurology · 2024Article
- Advances in CaChannels (Austin, Tex.) · 2023Review
- CaHandbook of experimental pharmacology · 2023Article
- CACNA1D-Related Channelopathies: From Hypertension to Autism.Handbook of experimental pharmacology · 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
- Ion-pair interactions between voltage-sensing domain IV and pore domain I regulate CaBiophysical journal · 2021Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors.
Funding
Abstract
The Ca(2+) channel alpha(1S) subunit (Ca(V)1.1) is the voltage sensor in skeletal muscle excitation-contraction (EC) coupling. Upon membrane depolarization, this sensor rapidly triggers Ca(2+) release from internal stores and conducts a slowly activating Ca(2+) current. However, this Ca(2+) current is not essential for skeletal muscle EC coupling. Here, we identified a Ca(V)1.1 splice variant with greatly distinct current properties. The variant of the CACNA1S gene lacking exon 29 was expressed at low levels in differentiated human and mouse muscle, and up to 80% in myotubes. To test its biophysical properties, we deleted exon 29 in a green fluorescent protein (GFP)-tagged alpha(1S) subunit and expressed it in dysgenic (alpha(1S)-null) myotubes. GFP-alpha(1S)Delta 29 was correctly targeted into triads and supported skeletal muscle EC coupling. However, the Ca(2+) currents through GFP-alpha(1S)Delta 29 showed a 30-mV left-shifted voltage dependence of activation and a substantially increased open probability, giving rise to an eightfold increased current density. This robust Ca(2+) influx contributed substantially to the depolarization-induced Ca(2+) transient that triggers contraction. Moreover, deletion of exon 29 accelerated current kinetics independent of the auxiliary alpha(2)delta-1 subunit. Thus, characterizing the Ca(V)1.1 Delta 29 splice variant revealed the structural bases underlying the specific gating properties of skeletal muscle Ca(2+) channels, and it suggests the existence of a distinct mode of EC coupling in developing muscle.
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