ArticleThe Journal of clinical investigation2006
CFTR is required for PKA-regulated ATP sensitivity of Kir1.1 potassium channels in mouse kidney.
Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 72 citations in OpenAlex.
- Article
- Kir6.1 and SUR2B in Cantú syndrome.American journal of physiology. Cell physiology · 2022Review
- Routes for Potassium Ions across Mitochondrial Membranes: A Biophysical Point of View with Special Focus on the ATP-Sensitive KBiomolecules · 2021Review
- Differential diagnosis of perinatal Bartter, Bartter and Gitelman syndromes.Clinical kidney journal · 2021Review
- Factoring in the Complexity of the Cystic Fibrosis Lung to UnderstandPathogens (Basel, Switzerland) · 2020Review
- Review
- Cystic fibrosis lung environment and Pseudomonas aeruginosa infection.BMC pulmonary medicine · 2016Review
- Article
- Animal Models of Cystic Fibrosis Pathology: Phenotypic Parallels and Divergences.BioMed research international · 2016Review
- Thick ascending limb of the loop of Henle.Clinical journal of the American Society of Nephrology : CJASN · 2014Review
- Genotype-specific alterations in vascular smooth muscle cell function in cystic fibrosis piglets.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2014Article
- Regulation of transport in the connecting tubule and cortical collecting duct.Comprehensive Physiology · 2012Review
- Human amnion epithelial cells induced to express functional cystic fibrosis transmembrane conductance regulator.PloS one · 2012Article
- Transit defect of potassium-chloride Co-transporter 3 is a major pathogenic mechanism in hereditary motor and sensory neuropathy with agenesis of the corpus callosum.The Journal of biological chemistry · 2011Article
- Regulation and function of potassium channels in aldosterone-sensitive distal nephron.Current opinion in nephrology and hypertension · 2010Review
- Cadmium regulates the expression of the CFTR chloride channel in human airway epithelial cells.Toxicological sciences : an official journal of the Society of Toxicology · 2010Article
- Molecular and functional characterization of the cystic fibrosis transmembrane conductance regulator from the Australian common brushtail possum, Trichosurus vulpecula.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2010Article
- CFTR chloride channel in the apical compartments: spatiotemporal coupling to its interacting partners.Integrative biology : quantitative biosciences from nano to macro · 2010Review
- Mouse cystic fibrosis transmembrane conductance regulator forms cAMP-PKA-regulated apical chloride channels in cortical collecting duct.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- A comprehensive guide to the ROMK potassium channel: form and function in health and disease.American journal of physiology. Renal physiology · 2009Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel plays vital roles in fluid transport in many epithelia. While CFTR is expressed along the entire nephron, its function in renal tubule epithelial cells remains unclear, as no specific renal phenotype has been identified in cystic fibrosis. CFTR has been proposed as a regulator of the 30 pS, ATP-sensitive renal K channel (Kir1.1, also known as renal outer medullar K [ROMK]) that is critical for K secretion by cells of the thick ascending limb (TAL) and distal nephron segments responsive to aldosterone. We report here that both ATP and glibenclamide sensitivities of the 30 pS K channel in TAL cells were absent in mice lacking CFTR and in mice homozygous for the deltaF508 mutation. Curcumin treatment in deltaF508-CFTR mice partially reversed the defect in ATP sensitivity. We demonstrate that the effect of CFTR on ATP sensitivity was abrogated by increasing PKA activity. We propose that CFTR regulates the renal K secretory channel by providing a PKA-regulated functional switch that determines the distribution of open and ATP-inhibited K channels in apical membranes. We discuss the potential physiological role of this functional switch in renal K handling during water diuresis and the relevance to renal K homeostasis in cystic fibrosis.
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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.