@prefix dcterms: . @prefix go: . @prefix this: . @prefix sub: . @prefix beldoc: . @prefix rdfs: . @prefix rdf: . @prefix xsd: . @prefix dce: . @prefix pav: . @prefix np: . @prefix belv: . @prefix prov: . @prefix schem: . @prefix Protein: . @prefix mgi: . @prefix geneProductOf: . @prefix species: . @prefix occursIn: . @prefix mesh: . @prefix pubmed: . @prefix orcid: . sub:Head { this: np:hasAssertion sub:assertion; np:hasProvenance sub:provenance; np:hasPublicationInfo sub:pubinfo; a np:Nanopublication . } sub:assertion { sub:_1 geneProductOf: mgi:88388; a Protein: . sub:_2 belv:translocationFrom go:0005622; belv:translocationOf schem:Chloride%281-%29; belv:translocationTo go:0005576 . sub:_3 rdf:object sub:_2; rdf:predicate belv:increases; rdf:subject sub:_1; a rdf:Statement . sub:_4 occursIn: mesh:D004848, species:10090; rdf:object sub:_3; rdf:predicate belv:increases; rdf:subject schem:cyclic%20AMP; a rdf:Statement . sub:assertion rdfs:label "a(SCHEM:\"cyclic AMP\") -> (p(MGI:Cftr) -> sec(a(SCHEM:\"Chloride(1-)\")))", "p(MGI:Cftr) -> sec(a(SCHEM:\"Chloride(1-)\"))" . } sub:provenance { beldoc: dce:description "Approximately 61,000 statements."; dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved."; dce:title "BEL Framework Large Corpus Document"; pav:authoredBy sub:_6; pav:version "1.4" . sub:_5 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."; prov:wasQuotedFrom pubmed:11741811 . sub:_6 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:11741811; prov:wasDerivedFrom beldoc:, sub:_5 . } sub:pubinfo { this: dcterms:created "2014-07-03T14:29:59.531+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }