ArticleThe Journal of physiology1998
Cl- transport by cystic fibrosis transmembrane conductance regulator (CFTR) contributes to the inhibition of epithelial Na+ channels (ENaCs) in Xenopus oocytes co-expressing CFTR and ENaC.
Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 119 citations in OpenAlex.
- Chloride channels and mast cell function: pioneering new frontiers in IBD therapy.Molecular and cellular biochemistry · 2025Review
- Review
- The Effect of Dynasore Upon the Negative Interaction Between ENaC and CFTR Channels in Xenopus laevis Oocytes.The Journal of membrane biology · 2022Article
- Cystic Fibrosis-Related Diabetes (CFRD): Overview of Associated Genetic Factors.Diagnostics (Basel, Switzerland) · 2021Review
- Abundant Monovalent Ions as Environmental Signposts for Pathogens during Host Colonization.Infection and immunity · 2021Review
- Lipid Nanoparticle-Delivered Chemically Modified mRNA Restores Chloride Secretion in Cystic Fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- CFTR/ENaC-dependent regulation of membrane potential during human sperm capacitation is initiated by bicarbonate uptake through NBC.The Journal of biological chemistry · 2018Article
- Chitosan in Non-Viral Gene Delivery: Role of Structure, Characterization Methods, and Insights in Cancer and Rare Diseases Therapies.Polymers · 2018Review
- Cystic Fibrosis-Related Diabetes.Frontiers in endocrinology · 2018Review
- Direct interactions between ENaC gamma subunit and ClCN2 in cystic fibrosis epithelial cells.Physiological reports · 2015Article
- Cystic fibrosis: an inherited disease affecting mucin-producing organs.The international journal of biochemistry & cell biology · 2014Review
- CFTR and TNR-CFTR expression and function in the kidney.Biophysical reviews · 2014Review
- Pouring salt on a wound: Pseudomonas aeruginosa virulence factors alter Na+ and Cl- flux in the lung.Journal of bacteriology · 2013Review
- 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
- Genetic variation of SCNN1A influences lung diffusing capacity in cystic fibrosis.Medicine and science in sports and exercise · 2012Article
- Cell and gene therapy for genetic diseases: inherited disorders affecting the lung and those mimicking sudden infant death syndrome.Human gene therapy · 2012Review
- ENaCs and ASICs as therapeutic targets.American journal of physiology. Cell physiology · 2012Review
- Contribution of casein kinase 2 and spleen tyrosine kinase to CFTR trafficking and protein kinase A-induced activity.Molecular and cellular biology · 2011Article
- Understanding protein kinase CK2 mis-regulation upon F508del CFTR expression.Naunyn-Schmiedeberg's archives of pharmacology · 2011Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Epithelial Na+ channels (ENaCs) are inhibited by the cystic fibrosis transmembrane conductance regulator (CFTR) when CFTR is activated by protein kinase A. Since cAMP-dependent activation of CFTR Cl- conductance is defective in cystic fibrosis (CF), ENaC currents are not inhibited by CFTR. This could explain the enhanced Na+ conductance found in CF. In the present study, we examined possible mechanisms of interaction between CFTR and ENaC co-expressed in Xenopus oocytes. 2. The magnitude of CFTR Cl- currents activated by 3-isobutyl-1-methylxanthine (IBMX) in oocytes co-expressing either wild-type or mutant CFTR and ENaC determined the degree of downregulation of ENaC currents. 3. The ability of CFTR to inhibit ENaC currents was significantly reduced either when extracellular Cl- was replaced by poorly conductive anions, e.g. SCN- or gluconate, or when CFTR was inhibited by diphenylamine-carboxylate (DPC, 1 mmol l-1). 4. Downregulation of ENaC was more pronounced at positive when compared with negative clamp voltages. This suggests that outward currents, i.e. influx of Cl- through activated CFTR most effectively downregulated ENaC. 5. Activation of endogenous Ca2+-activated Cl- currents by 1 micromol l-1 ionomycin did not inhibit ENaC current. This suggests that inhibition of ENaC mediated by Cl- currents may be specific to CFTR. 6. The present findings indicate that downregulation of ENaC by CFTR is correlated to the ability of CFTR to conduct Cl-. The data have implications for how epithelia switch from NaCl absorption to NaCl secretion when CFTR is activated by secretagogues.
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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.