ArticleThe Journal of general physiology2000
Role of domain 4 in sodium channel slow inactivation.
Article in The Journal of general physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 75 citations in OpenAlex.
- Electrophysiological characteristics of a SCN5A voltage sensors mutation R1629Q associated with Brugada syndrome.PloS one · 2013Trial
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- Fifty years of gating currents and channel gating.The Journal of general physiology · 2023Review
- Using voltage-sensor toxins and their molecular targets to investigate NaThe Journal of physiology · 2018Review
- Substitutions of the S4DIV R2 residue (R1451) in NaScientific reports · 2018Article
- N1366S mutation of human skeletal muscle sodium channel causes paramyotonia congenita.The Journal of physiology · 2017Article
- Modulatory features of the novel spider toxin μ-TRTX-Df1a isolated from the venom of the spider Davus fasciatus.British journal of pharmacology · 2017Article
- Pharmacology of the NaProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Defective fast inactivation recovery of Nav 1.4 in congenital myasthenic syndrome.Annals of neurology · 2015Article
- A gating model for wildtype and R1448H Nav1.4 channels in paramyotonia.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2014Article
- A gating charge interaction required for late slow inactivation of the bacterial sodium channel NavAb.The Journal of general physiology · 2013Article
- Voltage-sensor movements describe slow inactivation of voltage-gated sodium channels II: a periodic paralysis mutation in Na(V)1.4 (L689I).The Journal of general physiology · 2013Article
- Proton sensors in the pore domain of the cardiac voltage-gated sodium channel.The Journal of biological chemistry · 2013Article
- Gating transitions in the selectivity filter region of a sodium channel are coupled to the domain IV voltage sensor.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- NaChBac: the long lost sodium channel ancestor.Biochemistry · 2011Article
- Biophysical costs associated with tetrodotoxin resistance in the sodium channel pore of the garter snake, Thamnophis sirtalis.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2011Article
- Antillatoxin, a novel lipopeptide, enhances neurite outgrowth in immature cerebrocortical neurons through activation of voltage-gated sodium channels.The Journal of pharmacology and experimental therapeutics · 2010Article
- Slow inactivation of the NaV1.4 sodium channel in mammalian cells is impeded by co-expression of the beta1 subunit.Pflugers Archiv : European journal of physiology · 2009Article
- Sodium channel activation augments NMDA receptor function and promotes neurite outgrowth in immature cerebrocortical neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- A conserved ring of charge in mammalian Na+ channels: a molecular regulator of the outer pore conformation during slow inactivation.The Journal of physiology · 2006Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Depolarization of sodium channels initiates at least three gating pathways: activation, fast inactivation, and slow inactivation. Little is known about the voltage sensors for slow inactivation, a process believed to be separate from fast inactivation. Covalent modification of a cysteine substituted for the third arginine (R1454) in the S4 segment of the fourth domain (R3C) with negatively charged methanethiosulfonate-ethylsulfonate (MTSES) or with positively charged methanethiosulfonate-ethyltrimethylammonium (MTSET) produces a marked slowing of the rate of fast inactivation. However, only MTSES modification produces substantial effects on the kinetics of slow inactivation. Rapid trains of depolarizations (2-20 Hz) cause a reduction of the peak current of mutant channels modified by MTSES, an effect not observed for wild-type or unmodified R3C channels, or for mutant channels modified by MTSET. The data suggest that MTSES modification of R3C enhances entry into a slow-inactivated state, and also that the effects on slow inactivation are independent of alterations of either activation or fast inactivation. This effect of MTSES is observed only for cysteine mutants within the middle of this S4 segment, and the data support a helical secondary structure of S4 in this region. Mutation of R1454 to the negatively charged residues aspartate or glutamate cannot reproduce the effects of MTSES modification, indicating that charge alone cannot account for these results. A long-chained derivative of MTSES has similar effects as MTSES, and can produce these effects on a residue that does not show use-dependent current reduction after modification by MTSES, suggesting that the sulfonate moiety can reach a critical site affecting slow inactivation. The effects of MTSES on R3C are partially counteracted by a point mutation (W408A) that inhibits slow inactivation. Our data suggest that a region near the midpoint of the S4 segment of domain 4 plays an important role in slow inactivation.
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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.