ArticlePflugers Archiv : European journal of physiology2010
Control of volume-sensitive chloride channel inactivation by the coupled action of intracellular chloride and extracellular protons.
Article in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- A conserved mechanism of LRRC8 channel inhibition by two structurally distinct drugs.Communications biology · 2025Article
- Physiological Functions of the Volume-Regulated Anion Channel VRAC/LRRC8 and the Proton-Activated Chloride Channel ASOR/TMEM206.Handbook of experimental pharmacology · 2024Article
- cGAMP the travelling messenger.Frontiers in immunology · 2023Review
- Gating and anion selectivity are reciprocally regulated in TMEM16A (ANO1).The Journal of general physiology · 2022Article
- A 30-year journey from volume-regulated anion currents to molecular structure of the LRRC8 channel.The Journal of general physiology · 2019Review
- LRRC8 N termini influence pore properties and gating of volume-regulated anion channels (VRACs).The Journal of biological chemistry · 2018Article
- Phosphatidylinositol 4,5-bisphosphate, cholesterol, and fatty acids modulate the calcium-activated chloride channel TMEM16A (ANO1).Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Article
- Extracellular protons enable activation of the calcium-dependent chloride channel TMEM16A.The Journal of physiology · 2017Article
- Revealing the activation pathway for TMEM16A chloride channels from macroscopic currents and kinetic models.Pflugers Archiv : European journal of physiology · 2016Article
- VRAC: molecular identification as LRRC8 heteromers with differential functions.Pflugers Archiv : European journal of physiology · 2016Review
- Gating the glutamate gate of CLC-2 chloride channel by pore occupancy.The Journal of general physiology · 2016Article
- Gating modes of calcium-activated chloride channels TMEM16A and TMEM16B.The Journal of physiology · 2015Article
- Permeant anions contribute to voltage dependence of ClC-2 chloride channel by interacting with the protopore gate.The Journal of physiology · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The volume-sensitive chloride current (I(ClVol)) exhibit a time-dependent decay presumably due to channel inactivation. In this work, we studied the effects of chloride ions (Cl(-)) and H(+) ions on I(ClVol) decay recorded in HEK-293 and HL-60 cells using the whole-cell patch clamp technique. Under control conditions ([Cl(-)](e) = [Cl(-)](i) = 140 mM and pH(i) = pH(e) = 7.3), I(ClVol) in HEK cells shows a large decay at positive voltages but in HL-60 cells I(ClVol) remained constant independently of time. In HEK-293 cells, simultaneously raising the [Cl(-)](e) and [Cl(-)](i) from 25 to 140 mM (with pH(e) = pH(i) = 7.3) increased the fraction of inactivated channels (FIC). This effect was reproduced by elevating [Cl(-)](i) while keeping the [Cl(-)](e) constant. Furthermore, a decrease in pH(e) from 7.3 to 5.5 accelerated current decay and increased FIC when [Cl(-)] was 140 mM but not 25 mM. In HL-60 cells, a slight I(ClVol) decay was seen when the pH(e) was reduced from 7.3 to 5.5. Our data show that inactivation of I(ClVol) can be controlled by changing either the Cl(-) or H(+) concentration or both. Based on our results and previously published data, we have built a model that explains VRAC inactivation. In the model the H(+) binding site is located outside the electrical field near the extracellular entry whilst the Cl(-) binding site is intracellular. The model depicts inactivation as a pore constriction that happens by simultaneous binding of H(+) and Cl(-) ions to the channel followed by a voltage-dependent conformational change that ultimately causes inactivation.
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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.