ArticleThe Journal of physiology2005
CFTR fails to inhibit the epithelial sodium channel ENaC expressed in Xenopus laevis oocytes.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 56 citations in OpenAlex.
- Review
- Cystic Fibrosis: A Journey through Time and Hope.International journal of molecular sciences · 2024Review
- Epithelial NaComprehensive Physiology · 2024Review
- CFTR dysfunction leads to defective bacterial eradication on cystic fibrosis airways.Frontiers in physiology · 2024Review
- The Effect of Dynasore Upon the Negative Interaction Between ENaC and CFTR Channels in Xenopus laevis Oocytes.The Journal of membrane biology · 2022Article
- Association of cystic fibrosis transmembrane conductance regulator with epithelial sodium channel subunits carrying Liddle's syndrome mutations.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Is the ENaC Dysregulation in CF an Effect of Protein-Lipid Interaction in the Membranes?International journal of molecular sciences · 2021Review
- An integrated mathematical epithelial cell model for airway surface liquid regulation by mechanical forces.Journal of theoretical biology · 2018Article
- Marked increases in mucociliary clearance produced by synergistic secretory agonists or inhibition of the epithelial sodium channel.Scientific reports · 2016Article
- Review
- ENaCs and ASICs as therapeutic targets.American journal of physiology. Cell physiology · 2012Review
- Functional interaction between CFTR and the sodium-phosphate co-transport type 2a in Xenopus laevis oocytes.PloS one · 2012Article
- Enhancement of alveolar epithelial sodium channel activity with decreased cystic fibrosis transmembrane conductance regulator expression in mouse lung.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Human cystic fibrosis airway epithelia have reduced Cl- conductance but not increased Na+ conductance.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Regulation of endogenous ENaC functional expression by CFTR and ΔF508-CFTR in airway epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- The cystic fibrosis transmembrane conductance regulator impedes proteolytic stimulation of the epithelial Na+ channel.The Journal of biological chemistry · 2010Article
- Review
- Defective organellar acidification as a cause of cystic fibrosis lung disease: reexamination of a recurring hypothesis.American journal of physiology. Lung cellular and molecular physiology · 2009Review
- Assessment of the CFTR and ENaC association.Molecular bioSystems · 2009Review
- Towards a virtual lung: multi-scale, multi-physics modelling of the pulmonary system.Philosophical transactions. Series A, Mathematical, physical, and engineering sciences · 2008Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cystic fibrosis transmembrane conductance regulator (CFTR) plays a crucial role in regulating fluid secretion by the airways, intestines, sweat glands and other epithelial tissues. It is well established that the CFTR is a cAMP-activated, nucleotide-dependent anion channel, but additional functions are often attributed to it, including regulation of the epithelial sodium channel (ENaC). The absence of CFTR-dependent ENaC inhibition and the resulting sodium hyperabsorption were postulated to be a major electrolyte transport abnormality in cystic fibrosis (CF)-affected epithelia. Several ex vivo studies, including those that used the Xenopus oocyte expression system, have reported ENaC inhibition by activated CFTR, but contradictory results have also been obtained. Because CFTR-ENaC interactions have important implications in the pathogenesis of CF, the present investigation was undertaken by our three independent laboratories to resolve whether CFTR regulates ENaC in oocytes and to clarify potential sources of previously reported dissimilar observations. Using different experimental protocols and a wide range of channel expression levels, we found no evidence that activated CFTR regulates ENaC when oocyte membrane potential was carefully clamped. We determined that an apparent CFTR-dependent ENaC inhibition could be observed when resistance in series with the oocyte membrane was not low enough or the feedback voltage gain was not high enough. We suggest that the inhibitory effect of CFTR on ENaC reported in some earlier oocyte studies could be attributed to problems arising from high levels of channel expression and suboptimal recording conditions, that is, large series resistance and/or insufficient feedback voltage gain.
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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.