ArticleThe Journal of clinical investigation1996
Activation of endogenous deltaF508 cystic fibrosis transmembrane conductance regulator by phosphodiesterase inhibition.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 55 citations in OpenAlex.
- A novel drug series optimized to address cystic fibrosis and other CFTR deficiency diseases of human airways.npj drug discovery · 2025Article
- Changing the Paradigm - Treating the Basic Defect in Cystic Fibrosis.Indian journal of pediatrics · 2015Review
- Cystic fibrosis genetics: from molecular understanding to clinical application.Nature reviews. Genetics · 2015Review
- Anchored PDE4 regulates chloride conductance in wild-type and ΔF508-CFTR human airway epithelia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- PDE5 Inhibitors as Potential Tools in the Treatment of Cystic Fibrosis.Frontiers in pharmacology · 2012Article
- DeltaF508 CFTR processing correction and activity in polarized airway and non-airway cell monolayers.Pulmonary pharmacology & therapeutics · 2010Article
- Role of oxygen availability in CFTR expression and function.American journal of respiratory cell and molecular biology · 2008Article
- Targeted therapy for cystic fibrosis: cystic fibrosis transmembrane conductance regulator mutation-specific pharmacologic strategies.Molecular diagnosis & therapy · 2006Review
- Failure of cAMP agonists to activate rescued deltaF508 CFTR in CFBE41o- airway epithelial monolayers.The Journal of physiology · 2005Article
- Deletion of phenylalanine 508 causes attenuated phosphorylation-dependent activation of CFTR chloride channels.The Journal of physiology · 2000Article
- Strategies for correcting the delta F508 CFTR protein-folding defect.Journal of bioenergetics and biomembranes · 1997Review
- In vivo activation of the cystic fibrosis transmembrane conductance regulator mutant deltaF508 in murine nasal epithelium.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Many heterologously expressed mutants of the cystic fibrosis transmembrane conductance regulator (CFTR) exhibit residual chloride channel activity that can be stimulated by agonists of the adenylate cyclase/protein kinase A pathway. Because of clinical implications for cystic fibrosis of activating mutants in vivo, we are investigating whether deltaF508, the most common disease-associated CFTR mutation, can be activated in airway epithelial cells. We have found that, 36Cl- efflux can be stimulated 19-61% above baseline by beta-adrenoreceptor agonists and cGI-phosphodiesterase inhibitors in transformed nasal polyp (CF-T43) cells homozygous for the deltaF508 mutation. The increase in 36Cl- permeability is diminished by protein kinase A inhibitors and is not mediated by an increase in intracellular calcium concentrations. Preincubation of CF-T43 cells with CFTR anti-sense oligonucleotides prevented an increase in 36Cl- efflux in response to beta-agonist and phosphodiesterase inhibitor. Primary cells isolated from CF nasal polyps gave similar results. These data indicate that endogenous levels of deltaF508 protein can be stimulated to increase 36Cl- permeability in airway epithelial cells.
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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.