ArticleFrontiers in physiology2010
Physiology and pathophysiology of ClC-K/barttin channels.
Article in Frontiers in physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- A dual-organ genetic interplay between sensorineural hearing loss and kidney disease: an update for clinicians.Pediatric nephrology (Berlin, Germany) · 2026Review
- Description of the novel variant c.784delG;p. (Ala262Profs*68) atBiomedical reports · 2026Article
- Mechanism of Gating and Isoform-Specific Inhibition in Renal CLC Chloride Channels.bioRxiv : the preprint server for biology · 2026Article
- Expanding Genotype-Phenotype Correlation ofInternational journal of molecular sciences · 2023Article
- Small Molecules Targeting Kidney ClC-K Chloride Channels: Applications in Rare Tubulopathies and Common Cardiovascular Diseases.Biomolecules · 2023Review
- Inhibitory effect of S-nitroso-N-acetylpenicillamine on the basolateral 10-pS Cl- channel in thick ascending limb.PloS one · 2023Article
- Transcriptional profiling of transport mechanisms and regulatory pathways in rat choroid plexus.Fluids and barriers of the CNS · 2022Article
- Pathophysiological aspects of the thick ascending limb and novel genetic defects: HELIX syndrome and transient antenatal Bartter syndrome.Pediatric nephrology (Berlin, Germany) · 2022Review
- Bartter syndrome with long-term follow-up: a case report.The Journal of international medical research · 2020Article
- DHHC7-mediated palmitoylation of the accessory protein barttin critically regulates the functions of ClC-K chloride channels.The Journal of biological chemistry · 2020Article
- 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
- Thick Ascending Limb Sodium Transport in the Pathogenesis of Hypertension.Physiological reviews · 2019Review
- Reconstitution and NMR Characterization of the Ion-Channel Accessory Subunit Barttin in Detergents and Lipid-Bilayer Nanodiscs.Frontiers in molecular biosciences · 2019Article
- Renal Tubular Acidosis: HAdvances in chronic kidney disease · 2018Review
- Activation of renal ClC-K chloride channels depends on an intact N terminus of their accessory subunit barttin.The Journal of biological chemistry · 2018Article
- Bartter syndrome: causes, diagnosis, and treatment.International journal of nephrology and renovascular disease · 2018Review
- Functional severity of CLCNKB mutations correlates with phenotypes in patients with classic Bartter's syndrome.The Journal of physiology · 2017Article
- In silico model of the human ClC-Kb chloride channel: pore mapping, biostructural pathology and drug screening.Scientific reports · 2017Article
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ClC-K channels form a subgroup of anion channels within the ClC family of anion transport proteins. They are expressed predominantly in the kidney and in the inner ear, and are necessary for NaCl resorption in the loop of Henle and for K+ secretion by the stria vascularis. Subcellular distribution as well as the function of these channels are tightly regulated by an accessory subunit, barttin. Barttin improves the stability of ClC-K channel protein, stimulates the exit from the endoplasmic reticulum and insertion into the plasma membrane and changes its function by modifying voltage-dependent gating processes. The importance of ClC-K/barttin channels is highlighted by several genetic diseases. Dysfunctions of ClC-K channels result in Bartter syndrome, an inherited human condition characterized by impaired urinary concentration. Mutations in the gene encoding barttin, BSND, affect the urinary concentration as well as the sensory function of the inner ear. Surprisingly, there is one BSND mutation that causes deafness without affecting renal function, indicating that kidney function tolerates a reduction of anion channel activity that is not sufficient to support normal signal transduction in inner hair cells. This review summarizes recent work on molecular mechanisms, physiology, and pathophysiology of ClC-K/barttin channels.
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