ArticleProceedings of the National Academy of Sciences of the United States of America1999
The first-nucleotide binding domain of the cystic-fibrosis transmembrane conductance regulator is important for inhibition of the epithelial Na+ channel.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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
26 citing papers in PubMed.
- Human induced pluripotent stem cells for in vitro modeling of impaired mucociliary clearance in cystic fibrosis lung disease.Stem cell research & therapy · 2025Article
- Impaired Regulatory Volume Decrease and Characterization of Underlying Volume-Activated Currents in Cystic Fibrosis Human Cholangiocyte Cell Line.The Journal of membrane biology · 2022Article
- Article
- Impact ofJournal of ginseng research · 2019Article
- SPLUNC1 degradation by the cystic fibrosis mucosal environment drives airway surface liquid dehydration.The European respiratory journal · 2018Article
- Pulmonary epithelial barrier function: some new players and mechanisms.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Does epithelial sodium channel hyperactivity contribute to cystic fibrosis lung disease?The Journal of physiology · 2013Review
- Electrophysiological evidence for the presence of cystic fibrosis transmembrane conductance regulator (CFTR) in mouse sperm.Journal of cellular physiology · 2013Article
- Proteases, cystic fibrosis and the epithelial sodium channel (ENaC).Cell and tissue research · 2013Review
- Status of fluid and electrolyte absorption in cystic fibrosis.Cold Spring Harbor perspectives in medicine · 2013Article
- Assessing the Disease-Liability of Mutations in CFTR.Cold Spring Harbor perspectives in medicine · 2012Article
- Flow cytometry analysis reveals a decrease in intracellular sodium during sperm capacitation.Journal of cell science · 2012Article
- Introduction to section IV: biophysical methods to approach CFTR structure.Methods in molecular biology (Clifton, N.J.) · 2011Article
- Regulation of the epithelial Na+ channel and airway surface liquid volume by serine proteases.Pflugers Archiv : European journal of physiology · 2010Review
- Rescue of CF airway epithelial cell function in vitro by a CFTR potentiator, VX-770.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Mutation-specific potency and efficacy of cystic fibrosis transmembrane conductance regulator chloride channel potentiators.The Journal of pharmacology and experimental therapeutics · 2009Article
- Understanding the molecular basis of the interaction between NDPK-A and AMPK alpha 1.Molecular and cellular biology · 2006Article
- CFTR fails to inhibit the epithelial sodium channel ENaC expressed in Xenopus laevis oocytes.The Journal of physiology · 2005Article
- Lung infections associated with cystic fibrosis.Clinical microbiology reviews · 2002Review
- Molecular basis for defective glycosylation and Pseudomonas pathogenesis in cystic fibrosis lung.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cystic-fibrosis transmembrane conductance regulator (CFTR) functions as a cAMP-regulated Cl- channel and as a regulator of other membrane conductances. cAMP-dependent activation of CFTR inhibits epithelial Na+ channels (ENaC). The specificity of interaction between CFTR and ENaC was examined by coexpression of ENaC and ATP-binding cassette (ABC) proteins other than CFTR. In addition, we identified domains within CFTR that are of particular importance for the inhibition of ENaC. To that end, two-electrode voltage-clamp experiments were performed on Xenopus oocytes coexpressing ENaC together with CFTR, the multidrug resistance protein MDR1, the sulfonyl urea receptor SUR1, or the cadmium permease YCF1. Except for CFTR, none of the other ABC proteins were able to inhibit ENaC. Several truncated versions of CFTR were examined for their inhibitory effects on ENaC. In fact, it is shown that C-terminal truncated CFTR is able to inhibit ENaC on activation by intracellular cAMP. Moreover, the data also show that an intact first-nucleotide binding domain (NBF-1) is important for inhibition of ENaC. We conclude that NBF-1 of CFTR contains a CFTR-specific regulatory site that down-regulates ENaC. It is speculated that this regulatory site also is needed for CFTR-mediated interactions with other membrane proteins and that it is not present in NBF-1 of other ABC proteins.
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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.