@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 .
}