ArticleBiochimica et biophysica acta2014
I-J loop involvement in the pharmacological profile of CLC-K channels expressed in Xenopus oocytes.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Mechanism of Gating and Isoform-Specific Inhibition in Renal CLC Chloride Channels.bioRxiv : the preprint server for biology · 2026Article
- Pleiotropic Effects of the NSAID Fenamates on Chloride Channels: Opportunity for Ion Channelopathies?Pharmacology research & perspectives · 2025Review
- ClC-K Kidney Chloride Channels: From Structure to Pathology.Handbook of experimental pharmacology · 2024Article
- Small Molecules Targeting Kidney ClC-K Chloride Channels: Applications in Rare Tubulopathies and Common Cardiovascular Diseases.Biomolecules · 2023Review
- Functional Study of Novel Bartter's Syndrome Mutations in ClC-Kb and Rescue by the Accessory Subunit Barttin Toward Personalized Medicine.Frontiers in pharmacology · 2020Article
- New Insights into the Mechanism of NOJournal of the American Society of Nephrology : JASN · 2019Article
- In silico model of the human ClC-Kb chloride channel: pore mapping, biostructural pathology and drug screening.Scientific reports · 2017Article
- Pharmacovigilance database search discloses ClC-K channels as a novel target of the ATBritish journal of pharmacology · 2017Article
- Multidisciplinary study of a new ClC-1 mutation causing myotonia congenita: a paradigm to understand and treat ion channelopathies.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Regulatory-auxiliary subunits of CLC chloride channel-transport proteins.The Journal of physiology · 2015Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
CLC-K chloride channels and their subunit, barttin, are crucial for renal NaCl reabsorption and for inner ear endolymph production. Mutations in CLC-Kb and barttin cause Bartter syndrome. Here, we identified two adjacent residues, F256 and N257, that when mutated hugely alter in Xenopus oocytes CLC-Ka's biphasic response to niflumic acid, a drug belonging to the fenamate class, with F256A being potentiated 37-fold and N257A being potently blocked with a KD~1μM. These residues are localized in the same extracellular I-J loop which harbors a regulatory Ca(2+) binding site. This loop thus can represent an ideal and CLC-K specific target for extracellular ligands able to modulate channel activity. Furthermore, we demonstrated the involvement of the barttin subunit in the NFA potentiation. Indeed the F256A mutation confers onto CLC-K1 a transient potentiation induced by NFA which is found only when CLC-K1/F256A is co-expressed with barttin. Thus, in addition to the role of barttin in targeting and gating, the subunit participates in the pharmacological modulation of CLC-K channels and thus represents a further target for potential drugs.
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