ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Activation and inactivation of the voltage-gated sodium channel: role of segment S5 revealed by a novel hyperkalaemic periodic paralysis mutation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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
31 citing papers in PubMed, 82 citations in OpenAlex.
- Volatile anaesthetics modulate voltage-gated sodium channel function at a site directly linked to channel gating.Nature communications · 2026Article
- Exercise and fatigue: integrating the role of KEuropean journal of applied physiology · 2023Review
- Differential effects of modified batrachotoxins on voltage-gated sodium channel fast and slow inactivation.Cell chemical biology · 2022Article
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- Identification of aThe Journal of international medical research · 2020Article
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- Increased Resurgent Sodium Currents in Nav1.8 Contribute to Nociceptive Sensory Neuron Hyperexcitability Associated with Peripheral Neuropathies.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- A204E mutation in NaScientific reports · 2018Article
- Substitutions of the S4DIV R2 residue (R1451) in NaScientific reports · 2018Article
- SCN5A variant that blocks fibroblast growth factor homologous factor regulation causes human arrhythmia.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Enhanced slow inactivation of the human skeletal muscle sodium channel causing normokalemic periodic paralysis.Cellular and molecular neurobiology · 2014Article
- Proton sensors in the pore domain of the cardiac voltage-gated sodium channel.The Journal of biological chemistry · 2013Article
- Reduced Na(+) and higher K(+) channel expression and function contribute to right ventricular origin of arrhythmias in Scn5a+/- mice.Open biology · 2012Article
- Biophysical characterization of M1476I, a sodium channel founder mutation associated with cold-induced myotonia in French Canadians.The Journal of physiology · 2012Article
- Gating behaviour of sodium currents in adult mouse muscle recorded with an improved two-electrode voltage clamp.The Journal of physiology · 2011Article
- Skeletal muscle na channel disorders.Frontiers in pharmacology · 2011Article
- Article
- Four-mode gating model of fast inactivation of sodium channel Nav1.2a.Pflugers Archiv : European journal of physiology · 2008Article
- Mutations of sodium channel alpha-subunit genes in Chinese patients with normokalemic periodic paralysis.Cellular and molecular neurobiology · 2008Article
- A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity.The Journal of physiology · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Hyperkalaemic periodic paralysis, paramyotonia congenita, and potassium-aggravated myotonia are three autosomal dominant skeletal muscle disorders linked to the SCN4A gene encoding the alpha-subunit of the human voltage-sensitive sodium channel. To date, approximately 20 point mutations causing these disorders have been described. We have identified a new point mutation, in the SCN4A gene, in a family with a hyperkalaemic periodic paralysis phenotype. This mutation predicts an isoleucine-to-phenylalanine substitution at position 1495 located in the transmembrane segment S5 in the fourth homologous domain of the human alpha-subunit sodium channel. Introduction of the I1495F mutation into the wild-type channels disrupted the macroscopic current inactivation decay and shifted both steady-state activation and inactivation to the hyperpolarizing direction. The recovery from fast inactivation was slowed, and there was no effect on channel deactivation. Additionally, a significant enhancement of slow inactivation was observed in the I1495F mutation. In contrast, the T704M mutation, a hyperkalaemic periodic paralysis mutation located in the cytoplasmic interface of the S5 segment of the second domain, also shifted activation in the hyperpolarizing direction but had little effect on fast inactivation and dramatically impaired slow inactivation. These results, showing that the I1495F and T704M hyperkalaemic periodic paralysis mutations both have profound effects on channel activation and fast-slow inactivation, suggest that the S5 segment maybe in a location where fast and slow inactivation converge.
Indexed as
Identifiers
10366610PMC6782655W2108929466What 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.