ArticleBiophysical journal2013
Impaired gating of an L-Type Ca(2+) channel carrying a mutation linked to malignant hyperthermia.
Article in Biophysical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
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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.
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Who cites it
12 citing papers in PubMed.
- Pathogenic CaCommunications biology · 2026Article
- CaNature communications · 2024Article
- CaInternational journal of molecular sciences · 2022Review
- The distinct role of the four voltage sensors of the skeletal CaV1.1 channel in voltage-dependent activation.The Journal of general physiology · 2021Article
- Article
- Enhanced hippocampal type II theta activity AND altered theta architecture in mice lacking the CaScientific reports · 2021Article
- A Review of Genetic and Physiological Disease Mechanisms Associated With Cav1 Channels: Implications for Incomplete Congenital Stationary Night Blindness Treatment.Frontiers in genetics · 2021Article
- A skeletal muscle L-type CaThe Journal of biological chemistry · 2018Article
- Functional and structural characterization of a novel malignant hyperthermia-susceptible variant of DHPR-βAmerican journal of physiology. Cell physiology · 2018Article
- Distinct Components of Retrograde Ca(V)1.1-RyR1 Coupling Revealed by a Lethal Mutation in RyR1.Biophysical journal · 2016Article
- Channelopathies of skeletal muscle excitability.Comprehensive Physiology · 2015Review
- Structure-activity relationship of selected meta- and para-hydroxylated non-dioxin like polychlorinated biphenyls: from single RyR1 channels to muscle dysfunction.Toxicological sciences : an official journal of the Society of Toxicology · 2013Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors.
Funding
Abstract
Recently, we characterized the functional properties of a mutant skeletal muscle L-type Ca(2+) channel (CaV1.1 R174W) linked to the pharmacogenetic disorder malignant hyperthermia. Although the R174W mutation neutralizes the innermost basic amino acid in the voltage-sensing S4 helix of the first conserved membrane repeat of CaV1.1, the ability of the mutant channel to engage excitation-contraction coupling was largely unaffected by the introduction of the bulky tryptophan residue. In stark contrast, the mutation ablated the ability of CaV1.1 to produce L-type current under our standard recording conditions. In this study, we have investigated the mechanism of channel dysfunction more extensively. We found that CaV1.1 R174W will open and conduct Ca(2+) in response to strong or prolonged depolarizations in the presence of the 1,4-dihydropyridine receptor agonist ±Bay K 8644. From these results, we have concluded that the R174W mutation impedes entry into both mode 1(low Po) and mode 2 (high Po) gating states and that these gating impairments can be partially overcome by maneuvers that promote entry into mode 2.
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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.