ReviewBiochimica et biophysica acta2013
Ca(V)1.1: The atypical prototypical voltage-gated Ca²⁺ channel.
Review in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed.
- Efficacy of sodium channel blockers in treating myotonia is independent of action potential sodium current block.The Journal of physiology · 2026Article
- Early-life tobacco exposure elevating childhood attention-deficit hyperactivity disorder risk: a two-sample Mendelian randomisation analysis.European archives of psychiatry and clinical neuroscience · 2026Article
- Label-free morphology-based phenotypic analysis of spinal and bulbar muscular atrophy muscle cell models.Disease models & mechanisms · 2025Article
- ERG1A KScientific reports · 2025Article
- Inactivation of CaV1 and CaV2 channels.The Journal of general physiology · 2025Review
- Voltage sensors.Molecular pharmacology · 2025Review
- Neuromodulation influences T lymphocyte calcium signaling and alpha synuclein clearance: implications for Parkinson's disease.Frontiers in cellular neuroscience · 2025Review
- CaNature communications · 2024Article
- Spatial transcriptomics in embryonic mouse diaphragm muscle reveals regional gradients and subdomains of developmental gene expression.iScience · 2024Article
- Advances in CaChannels (Austin, Tex.) · 2023Review
- Biophysical reviews top five: voltage-dependent charge movement in nerve and muscle.Biophysical reviews · 2023Review
- Calmodulin Mutations in Human Disease.Channels (Austin, Tex.) · 2023Review
- Energy (and Reactive Oxygen Species Generation) Saving Distribution of Mitochondria for the Activation of ATP Production in Skeletal Muscle.Antioxidants (Basel, Switzerland) · 2023Review
- Endoplasmic Reticulum-Plasma Membrane Junctions as Sites of Depolarization-Induced CaAnnual review of physiology · 2023Review
- Probing ion binding in the selectivity filter of the CaBiophysical journal · 2023Article
- Modulation of L-type calcium channels in Alzheimer's disease: A potential therapeutic target.Computational and structural biotechnology journal · 2023Review
- Selective posttranslational inhibition of CaNature communications · 2022Article
- Proteomic profiling of impaired excitation-contraction coupling and abnormal calcium handling in muscular dystrophy.Proteomics · 2022Review
- Effects of progesterone on T-type-CaNeural regeneration research · 2022Article
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Ca(V)1.1 is the prototype for the other nine known Ca(V) channel isoforms, yet it has functional properties that make it truly atypical of this group. Specifically, Ca(V)1.1 is expressed solely in skeletal muscle where it serves multiple purposes; it is the voltage sensor for excitation-contraction coupling and it is an L-type Ca²⁺ channel which contributes to a form of activity-dependent Ca²⁺ entry that has been termed Excitation-coupled Ca²⁺ entry. The ability of Ca(V)1.1 to serve as voltage-sensor for excitation-contraction coupling appears to be unique among Ca(V) channels, whereas the physiological role of its more conventional function as a Ca²⁺ channel has been a matter of uncertainty for nearly 50 years. In this chapter, we discuss how Ca(V)1.1 supports excitation-contraction coupling, the possible relevance of Ca²⁺ entry through Ca(V)1.1 and how alterations of Ca(V)1.1 function can have pathophysiological consequences. This article is part of a Special Issue entitled: Calcium channels.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.