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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAulIv-rYSNHgKNWGZEFcS27ryN5ae4cZPrDAlCXRdmp4#_6 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAulIv-rYSNHgKNWGZEFcS27ryN5ae4cZPrDAlCXRdmp4#_5 http://www.w3.org/ns/prov#value We investigated adenosine (Ado) activation of the cystic fibrosis transmembrane conductance regulator (CFTR) in vitro and in vivo. A(2B) Ado receptors were identified in Calu-3, IB-3-1, COS-7, and primary human airway cells. Ado elevated cAMP in Calu-3, IB-3-1, and COS-7 cells and activated protein kinase A-dependent halide efflux in Calu-3 cells. Ado promoted arachidonic acid release from Calu-3 cells, and phospholipase A(2) (PLA(2)) inhibition blocked Ado-activated halide efflux in Calu-3 and COS-7 cells expressing CFTR. Forskolin- and beta(2)-adrenergic receptor-stimulated efflux were not affected by the same treatment. Cytoplasmic PLA(2) (cPLA(2)) was identified in Calu-3, IB-3-1, and COS-7 cells, but cPLA(2) inhibition did not affect Ado-stimulated cAMP concentrations. In cftr(+) and cftr(-/-) mice, Ado stimulated nasal Cl(-) secretion that was CFTR dependent and sensitive to A(2) receptor and PLA(2) blockade. In COS-7 cells transiently expressing DeltaF508 CFTR, Ado activated halide efflux. Ado also activated G551D CFTR-dependent halide efflux when combined with arachidonic acid and phosphodiesterase inhibition. In conclusion, PLA(2) and protein kinase A both contribute to A(2) receptor activation of CFTR, and components of this signaling pathway can augment wild-type and mutant CFTR activity. http://www.tkuhn.ch/bel2nanopub/RAulIv-rYSNHgKNWGZEFcS27ryN5ae4cZPrDAlCXRdmp4#_5 http://www.w3.org/ns/prov#wasQuotedFrom http://www.ncbi.nlm.nih.gov/pubmed/11741811 http://www.tkuhn.ch/bel2nanopub/RAulIv-rYSNHgKNWGZEFcS27ryN5ae4cZPrDAlCXRdmp4#_6 http://www.w3.org/2000/01/rdf-schema#label Selventa http://www.tkuhn.ch/bel2nanopub/RAulIv-rYSNHgKNWGZEFcS27ryN5ae4cZPrDAlCXRdmp4#assertion http://www.w3.org/ns/prov#hadPrimarySource http://www.ncbi.nlm.nih.gov/pubmed/11741811 http://www.tkuhn.ch/bel2nanopub/RAulIv-rYSNHgKNWGZEFcS27ryN5ae4cZPrDAlCXRdmp4#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://www.tkuhn.ch/bel2nanopub/RAulIv-rYSNHgKNWGZEFcS27ryN5ae4cZPrDAlCXRdmp4#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://www.tkuhn.ch/bel2nanopub/RAulIv-rYSNHgKNWGZEFcS27ryN5ae4cZPrDAlCXRdmp4#_5 http://www.tkuhn.ch/bel2nanopub/RAulIv-rYSNHgKNWGZEFcS27ryN5ae4cZPrDAlCXRdmp4#pubinfo http://www.tkuhn.ch/bel2nanopub/RAulIv-rYSNHgKNWGZEFcS27ryN5ae4cZPrDAlCXRdmp4 http://purl.org/dc/terms/created 2014-07-03T14:29:59.531+02:00 http://www.tkuhn.ch/bel2nanopub/RAulIv-rYSNHgKNWGZEFcS27ryN5ae4cZPrDAlCXRdmp4 http://purl.org/pav/createdBy http://orcid.org/0000-0001-6818-334X http://www.tkuhn.ch/bel2nanopub/RAulIv-rYSNHgKNWGZEFcS27ryN5ae4cZPrDAlCXRdmp4 http://purl.org/pav/createdBy http://orcid.org/0000-0002-1267-0234