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Gating pore currents in sodium channels
United States.
France.
KTH, School of Engineering Sciences (SCI), Applied Physics, Biophysics.ORCID iD: 0000-0002-0828-3899
2018 (English)In: Handbook of Experimental Pharmacology, ISSN 0171-2004, E-ISSN 1865-0325, p. 371-399Article in journal (Refereed) Published
Abstract [en]

Voltage-gated sodium channels belong to the superfamily of voltage-gated cation channels. Their structure is based on domains comprising a voltage sensor domain (S1–S4 segments) and a pore domain (S5–S6 segments). Mutations in positively charged residues of the S4 segments may allow protons or cations to pass directly through the gating pore constriction of the voltage sensor domain; these anomalous currents are referred to as gating pore or omega (ω) currents. In the skeletal muscle disorder hypokalemic periodic paralysis, and in arrhythmic dilated cardiomyopathy, inherited mutations of S4 arginine residues promote omega currents that have been shown to be a contributing factor in the pathogenesis of these sodium channel disorders. Characterization of gating pore currents in these channelopathies and with artificial mutations has been possible by measuring the voltage-dependence and selectivity of these leak currents. The basis of gating pore currents and the structural basis of S4 movement through the gating pore has also been studied extensively with molecular dynamics. These simulations have provided valuable insight into the nature of S4 translocation and the physical basis for the effects of mutations that promote permeation of protons or cations through the gating pore.

Place, publisher, year, edition, pages
Springer, 2018. p. 371-399
Keywords [en]
Arrhythmic dilated cardiomyopathy, Gating pore, Hypokalemic periodic paralysis, Molecular dynamics, Omega current, Sodium channel, acetazolamide, diclofenamide, sodium channel Nav1.4, sodium channel Nav1.5, voltage gated sodium channel, action potential, cardiac channelopathy, channel gating, congestive cardiomyopathy, drug efficacy, gating pore current, gene mutation, human, nonhuman, phenotype, priority journal, sodium channelopathy, sodium current, animal, channelopathy, chemistry, genetics, mutation, physiology, Action Potentials, Animals, Channelopathies, Humans, Ion Channel Gating, Voltage-Gated Sodium Channels
National Category
Condensed Matter Physics
Identifiers
URN: urn:nbn:se:kth:diva-236448DOI: 10.1007/164_2017_54Scopus ID: 2-s2.0-85048200099OAI: oai:DiVA.org:kth-236448DiVA, id: diva2:1257506
Note

QC 20181022

Available from: 2018-10-22 Created: 2018-10-22 Last updated: 2018-10-30Bibliographically approved

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Delemotte, Lucie

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