ArticleProceedings of the National Academy of Sciences of the United States of America1992
A1 adenosine-receptor antagonists activate chloride efflux from cystic fibrosis cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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, 89 citations in OpenAlex.
- Ethanol-Induced Cerebellar Ataxia: Cellular and Molecular Mechanisms.Cerebellum (London, England) · 2015Article
- Activation of 3-phosphoinositide-dependent kinase 1 (PDK1) and serum- and glucocorticoid-induced protein kinase 1 (SGK1) by short-chain sphingolipid C4-ceramide rescues the trafficking defect of ΔF508-cystic fibrosis transmembrane conductance regulator (ΔF508-CFTR).The Journal of biological chemistry · 2014Article
- Cystic fibrosis transmembrane regulator correctors and potentiators.Cold Spring Harbor perspectives in medicine · 2013Review
- Physical Characterization of 1,3-dipropyl-8-cyclopentylxanthine (CPX).AAPS PharmSciTech · 2010Article
- Review
- Purinergic receptors in the endocrine and exocrine pancreas.Purinergic signalling · 2008Article
- Adenosine receptors in rat and human pancreatic ducts stimulate chloride transport.Pflugers Archiv : European journal of physiology · 2008Article
- Amphiphilic pyridinium salts block TNF alpha/NF kappa B signaling and constitutive hypersecretion of interleukin-8 (IL-8) from cystic fibrosis lung epithelial cells.Biochemical pharmacology · 2005Article
- Digitoxin mimics gene therapy with CFTR and suppresses hypersecretion of IL-8 from cystic fibrosis lung epithelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- General anesthetic octanol and related compounds activate wild-type and delF508 cystic fibrosis chloride channels.British journal of pharmacology · 2004Article
- Comparative pharmacology of the activity of wild-type and G551D mutated CFTR chloride channel: effect of the benzimidazolone derivative NS004.The Journal of membrane biology · 2003Article
- Correction of G551D-CFTR transport defect in epithelial monolayers by genistein but not by CPX or MPB-07.British journal of pharmacology · 2002Article
- Pharmacogenomics of cystic fibrosis.Molecular interventions · 2001Review
- Pharmacogenomics of the cystic fibrosis transmembrane conductance regulator (CFTR) and the cystic fibrosis drug CPX using genome microarray analysis.Molecular medicine (Cambridge, Mass.) · 1999Article
- Direct activation of cystic fibrosis transmembrane conductance regulator channels by 8-cyclopentyl-1,3-dipropylxanthine (CPX) and 1,3-diallyl-8-cyclohexylxanthine (DAX).The Journal of biological chemistry · 1998Article
- 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
- delta F508 in cystic fibrosis: willing but not able.Archives of disease in childhood · 1997Review
- Activation of endogenous deltaF508 cystic fibrosis transmembrane conductance regulator by phosphodiesterase inhibition.The Journal of clinical investigation · 1996Article
- CPX, a selective A1-adenosine-receptor antagonist, regulates intracellular pH in cystic fibrosis cells.The American journal of physiology · 1995Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
A1 adenosine-receptor-antagonist drugs such as 8-cyclopentyl-1,3-dipropylxanthine (CPX) and xanthine amine congener (XAC) are found to activate the efflux of 36Cl- from CFPAC cells. These cells are a pancreatic adenocarcinoma cell line derived from a cystic fibrosis (CF) patient homozygous for the common mutation, deletion of Phe-508. The active concentrations for these compounds are in the low nanomolar range, consistent with action on A1 adenosine receptors. In addition, drug action can be blocked by exogenous agonists such as 2-chloroadenosine and also can be antagonized by removal of endogenous agonists by treatment with adenosine deaminase. Cells lacking the CF genotype and phenotype, such as HT-29 and T84 colon carcinoma cell lines, appear to be resistant to activation of chloride efflux by either drug. CFPAC cells transfected with the CF transmembrane regulator gene, CFTR, are also resistant to activation by CPX. We conclude that, since these antagonists are of relatively low toxicity and appear to act somewhat selectively, they might be considered as promising therapeutic candidates for CF.
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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.