ArticleThe Journal of physiology2005
Charge immobilization of the voltage sensor in domain IV is independent of sodium current inactivation.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Molecular basis of sodium channel inactivation.Nature communications · 2025Article
- Potential C-terminal domain interactions of the cardiac voltage gated sodium channel.Scientific reports · 2025Article
- Conformations of voltage-sensing domain III differentially define NaV channel closed- and open-state inactivation.The Journal of general physiology · 2021Review
- Mechanisms of noncovalent β subunit regulation of NaThe Journal of general physiology · 2017Article
- Molecular Pathophysiology of Congenital Long QT Syndrome.Physiological reviews · 2017Review
- The hitchhiker's guide to the voltage-gated sodium channel galaxy.The Journal of general physiology · 2016Review
- Direct Measurement of Cardiac Na+ Channel Conformations Reveals Molecular Pathologies of Inherited Mutations.Circulation. Arrhythmia and electrophysiology · 2015Article
- Sequence variations at I260 and A1731 contribute to persistent currents in Drosophila sodium channels.Neuroscience · 2014Article
- Sodium channels as gateable non-photonic sensors for membrane-delimited reactive species.Biochimica et biophysica acta · 2014Article
- Extracellular protons inhibit charge immobilization in the cardiac voltage-gated sodium channel.Biophysical journal · 2013Article
- Molecular basis for class Ib anti-arrhythmic inhibition of cardiac sodium channels.Nature communications · 2011Article
- Lidocaine partially depolarizes the S4 segment in domain IV of the sodium channel.Pflugers Archiv : European journal of physiology · 2011Article
- Evidence for multiple effects of ProTxII on activation gating in Na(V)1.5.Toxicon : official journal of the International Society on Toxinology · 2008Article
- More gating charges are needed to open a Shaker K+ channel than are needed to open an rBIIA Na+ channel.Biophysical journal · 2008Article
- Charge immobilization of skeletal muscle Na+ channels: role of residues in the inactivation linker.Biophysical journal · 2007Article
- Outward stabilization of the S4 segments in domains III and IV enhances lidocaine block of sodium channels.The Journal of physiology · 2007Article
- Central charged residues in DIIIS4 regulate deactivation gating in skeletal muscle sodium channels.Cellular and molecular neurobiology · 2007Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Recovery from fast inactivation in voltage-dependent Na+ channels is associated with a slow component in the time course of gating charge during repolarization (i.e. charge immobilization), which results from the slow movement of the S4 segments in domains III and IV (S4-DIII and S4-DIV). Previous studies have shown that the non-specific removal of fast inactivation by the proteolytic enzyme pronase eliminated charge immobilization, while the specific removal of fast inactivation (by intracellular MTSET modification of a cysteine substituted for the phenylalanine in the IFM motif, ICMMTSET, in the inactivation particle formed by the linker between domains III and IV) only reduced the amount of charge immobilization by nearly one-half. To investigate the molecular origin of the remaining slow component of charge immobilization we studied the human cardiac Na+ channel (hH1a) in which the outermost arginine in the S4-DIV, which contributes approximately 20% to total gating charge (Qmax), was mutated to a cysteine (R1C-DIV). Gating charge could be fully restored in R1C-DIV by exposure to extracellular MTSEA, a positively charged methanethiosulphonate reagent. The RIC-DIV mutation was combined with ICMMTSET to remove fast inactivation, and the gating currents of R1C-DIV-ICM(MTSET) were recorded before and after modification with MTSEAo. Prior to MTSEAo, the time course of the gating charge during repolarization (off-charge) was best described by a single fast time constant. After MTSEA, the off-charge had both fast and slow components, with the slow component accounting for nearly 35% of Qmax. These results demonstrate that the slow movement of the S4-DIV during repolarization is not dependent upon the normal binding of the inactivation particle.
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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.