ArticleBiophysical journal2013
Alkaline pH block of CLC-K kidney chloride channels mediated by a pore lysine residue.
Article in Biophysical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- ClC-K Kidney Chloride Channels: From Structure to Pathology.Handbook of experimental pharmacology · 2024Article
- Role of PKC in the Regulation of the Human Kidney Chloride Channel ClC-Ka.Scientific reports · 2020Article
- Proton-dependent inhibition, inverted voltage activation, and slow gating of CLC-0 Chloride Channel.PloS one · 2020Article
- Mutation of external glutamate residue reveals a new intermediate transport state and anion binding site in a CLC ClProceedings of the National Academy of Sciences of the United States of America · 2019Article
- A selective class of inhibitors for the CLC-Ka chloride ion channel.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Pharmacovigilance database search discloses ClC-K channels as a novel target of the ATBritish journal of pharmacology · 2017Article
- New perspective of ClC-Kb/2 Cl- channel physiology in the distal renal tubule.American journal of physiology. Renal physiology · 2016Review
- A Novel Mechanism of pH Buffering in C. elegans Glia: Bicarbonate Transport via the Voltage-Gated ClC Cl- Channel CLH-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- I-J loop involvement in the pharmacological profile of CLC-K channels expressed in Xenopus oocytes.Biochimica et biophysica acta · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
CLC-K chloride channels are expressed in the kidney and the inner ear, where they are involved in NaCl reabsorption and endolymph production, respectively. These channels require the beta subunit barttin for proper function. Mutations in ClC-Kb and barttin, lead to Bartter's syndrome. Block of CLC-K channels by acid pH was described in a previous work, and we had identified His-497 as being responsible for the acidic block of CLC-K channels. Here, we show that ClC-K currents are blocked also by alkaline pH with an apparent pK value of ∼8.7 for ClC-K1. Using noise analysis, we demonstrate that alkaline block is mediated by an allosteric reduction of the open probability. By an extensive mutagenic screen we identified K165, a highly conserved residue in the extracellular vestibule of the channel, as the major element responsible for the alkaline pH modulation. Deprotonation of K165 underlies the alkaline block. However, MTS modification of the K165C mutant demonstrated that not only the charge but also the chemical and sterical properties of lysine 165 are determinants of CLC-K gating.
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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.