ReviewFrontiers in pharmacology2014
Biophysics, pathophysiology, and pharmacology of ion channel gating pores.
Review in Frontiers in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed.
- Review
- The differential impacts of equivalent gating-charge mutations in voltage-gated sodium channels.The Journal of general physiology · 2025Article
- Mapping structural distribution and gating-property impacts of disease-associated mutations in voltage-gated sodium channels.iScience · 2024Article
- ELUCIDATING THE DIFFERENTIAL IMPACTS OF EQUIVALENT GATING-CHARGE MUTATIONS IN VOLTAGE-GATED SODIUM CHANNELS.bioRxiv : the preprint server for biology · 2024Article
- Pathogenic gating pore current conducted by autism-related mutations in the NaProceedings of the National Academy of Sciences of the United States of America · 2024Article
- An LQT2-related mutation in the voltage-sensing domain is involved in switching the gating polarity of hERG.BMC biology · 2024Article
- Exploring Flexibility and Folding Patterns Throughout Time in Voltage Sensors.Journal of molecular evolution · 2023Article
- Characterization of two pathological gating-charge substitutions in Cav1.4 L-type calcium channels.Channels (Austin, Tex.) · 2023Article
- Ion currents through the voltage sensor domain of distinct families of proteins.Journal of biological physics · 2023Review
- Domain- and state-specific shape of the electric field tunes voltage sensing in voltage-gated sodium channels.Biophysical journal · 2023Article
- Functional Characterization of Four Known Cav2.1 Variants Associated with Neurodevelopmental Disorders.Membranes · 2023Article
- Multifocal ectopic purkinje-related premature contractions and related cardiomyopathy.Frontiers in cardiovascular medicine · 2023Review
- A TRPM7 mutation linked to familial trigeminal neuralgia: Omega current and hyperexcitability of trigeminal ganglion neurons.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Development of an automated screen for Kv7.2 potassium channels and discovery of a new agonist chemotype.Bioorganic & medicinal chemistry letters · 2022Article
- Ratio of Hydrophobic-Hydrophilic and Positive-Negative Residues at Lipid-Water-Interface Influences Surface Expression and Channel Gating of TRPV1.The Journal of membrane biology · 2022Article
- Review
- Epilepsy Combined With Multiple Gene Heterozygous Mutation.Frontiers in pediatrics · 2022Article
- Photopharmacology of Ion Channels through the Light of the Computational Microscope.International journal of molecular sciences · 2021Review
- Analysis of an electrostatic mechanism for ΔpH dependent gating of the voltage-gated proton channel, HBiochimica et biophysica acta. Bioenergetics · 2021Review
- Kv3.1 channelopathy: a novel loss-of-function variant and the mechanistic basis of its clinical phenotypes.Annals of translational medicine · 2021Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage sensor domains (VSDs) are a feature of voltage gated ion channels (VGICs) and voltage sensitive proteins. They are composed of four transmembrane (TM) segments (S1-S4). Currents leaking through VSDs are called omega or gating pore currents. Gating pores are caused by mutations of the highly conserved positively charged amino acids in the S4 segment that disrupt interactions between the S4 segment and the gating charge transfer center (GCTC). The GCTC separates the intracellular and extracellular water crevices. The disruption of S4-GCTC interactions allows these crevices to communicate and create a fast activating and non-inactivating alternative cation-selective permeation pathway of low conductance, or a gating pore. Gating pore currents have recently been shown to cause periodic paralysis phenotypes. There is also increasing evidence that gating pores are linked to several other familial diseases. For example, gating pores in Nav1.5 and Kv7.2 channels may underlie mixed arrhythmias associated with dilated cardiomyopathy (DCM) phenotypes and peripheral nerve hyperexcitability (PNH), respectively. There is little evidence for the existence of gating pore blockers. Moreover, it is known that a number of toxins bind to the VSD of a specific domain of Na(+) channels. These toxins may thus modulate gating pore currents. This focus on the VSD motif opens up a new area of research centered on developing molecules to treat a number of cell excitability disorders such as epilepsy, cardiac arrhythmias, and pain. The purpose of the present review is to summarize existing knowledge of the pathophysiology, biophysics, and pharmacology of gating pore currents and to serve as a guide for future studies aimed at improving our understanding of gating pores and their pathophysiological roles.
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