ArticleThe Journal of physiology2002
Modulation of homomeric and heteromeric KCNQ1 channels by external acidification.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Cell Settling, Migration, and Stochastic Cancer Gene Expression Suggest Potassium Membrane Flux May Initiate pH Reversal.Biomolecules · 2025Article
- Cardiac Organoid Model Inspired Micro-Robot Smart Patch to Treat Myocardial Infarction.Advanced materials (Deerfield Beach, Fla.) · 2025Article
- The Physiology of the Gastric Parietal Cell.Physiological reviews · 2020Review
- Inactivation gating of Kv7.1 channels does not involve concerted cooperative subunit interactions.Channels (Austin, Tex.) · 2018Article
- Probing Structural Dynamics and Topology of the KCNE1 Membrane Protein in Lipid Bilayers via Site-Directed Spin Labeling and Electron Paramagnetic Resonance Spectroscopy.Biochemistry · 2015Article
- Polyunsaturated fatty acid analogs act antiarrhythmically on the cardiac IKs channel.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Article
- Towards bridging the gap between acid-base transporters and neuronal excitability modulation.International journal of physiology, pathophysiology and pharmacology · 2014Article
- Influence of pH on Ca²⁺ current and its control of electrical and Ca²⁺ signaling in ventricular myocytes.The Journal of general physiology · 2011Article
- Update on the mechanisms of gastric acid secretion.Current gastroenterology reports · 2010Review
- Article
- Regulation of wild-type and mutant KCNQ1/KCNE1 channels by tyrosine kinase.Pflugers Archiv : European journal of physiology · 2009Article
- Structure of KCNE1 and implications for how it modulates the KCNQ1 potassium channel.Biochemistry · 2008Article
- Extracellular pH modulates the voltage-dependent Ca2+ current and low threshold K+ current in hair cells.Neurochemical research · 2008Article
- An inactivation gate in the selectivity filter of KCNQ1 potassium channels.Biophysical journal · 2007Article
- Inactivation as a new regulatory mechanism for neuronal Kv7 channels.Biophysical journal · 2007Article
- External barium affects the gating of KCNQ1 potassium channels and produces a pore block via two discrete sites.The Journal of general physiology · 2004Article
- pH modulation of currents that contribute to the medium and slow afterhyperpolarizations in rat CA1 pyramidal neurones.The Journal of physiology · 2004Article
- Mechanisms underlying modulation of neuronal KCNQ2/KCNQ3 potassium channels by extracellular protons.The Journal of general physiology · 2003Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The I(KS) K(+) channel plays a major role in repolarizing the cardiac action potential. It consists of an assembly of two structurally distinct alpha and beta subunits called KCNQ1 and KCNE1, respectively. Using two different expression systems, Xenopus oocytes and Chinese hamster ovary cells, we investigated the effects of external protons on homomeric and heteromeric KCNQ1 channels. External acidification (from pH 7.4 to pH 5.5) markedly decreased the homomeric KCNQ1 current amplitude and caused a positive shift (+25 mV) in the voltage dependence of activation. Low external pH (pH(o)) also slowed down the activation and deactivation kinetics and strongly reduced the KCNQ1 inactivation process. In contrast, external acidification reduced the maximum conductance and the macroscopic inactivation of the KCNQ1 mutant L273F by only a small amount. The heteromeric I(KS) channel complex was weakly affected by low pH(o), with minor effects on I(KS) current amplitude. However, substantial current inhibition was produced by protons with the N-terminal KCNE1 deletion mutant Delta11-38. Low pH(o) increased the current amplitude of the pore mutant V319C when co-expressed with KCNE1. The slowing of I(KS) deactivation produced by low pH(o) was absent in the KCNE1 mutant Delta39-43, suggesting that the residues lying at the N-terminal boundary of the transmembrane segment are involved in this process. In all, our results suggest that external acidification acts on homomeric and heteromeric KCNQ1 channels via multiple mechanisms to affect gating and maximum conductance. The external pH effects on I(Kr) versus I(KS) may be important determinants of arrhythmogenicity under conditions of cardiac ischaemia and reperfusion.
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