@prefix dcterms: .
@prefix this: .
@prefix sub: .
@prefix beldoc: .
@prefix rdfs: .
@prefix rdf: .
@prefix xsd: .
@prefix dce: .
@prefix pav: .
@prefix np: .
@prefix belv: .
@prefix prov: .
@prefix go: .
@prefix ncm: .
@prefix ProteinComplex: .
@prefix hasAgent: .
@prefix Protein: .
@prefix pfm: .
@prefix geneProductOf: .
@prefix mesh: .
@prefix occursIn: .
@prefix species: .
@prefix pubmed: .
@prefix orcid: .
sub:Head {
this: np:hasAssertion sub:assertion;
np:hasProvenance sub:provenance;
np:hasPublicationInfo sub:pubinfo;
a np:Nanopublication .
}
sub:assertion {
ncm:p85%2Fp110%20PI3Kinase%20Complex a ProteinComplex: .
sub:_1 hasAgent: ncm:p85%2Fp110%20PI3Kinase%20Complex;
a go:0016301 .
sub:_2 hasAgent: sub:_3;
a go:0016301 .
sub:_3 geneProductOf: pfm:Akt%20Family;
a Protein: .
sub:_4 occursIn: mesh:D005347, mesh:D008168, species:10090;
rdf:object sub:_2;
rdf:predicate belv:increases;
rdf:subject sub:_1;
a rdf:Statement .
sub:assertion rdfs:label "kin(complex(NCM:\"p85/p110 PI3Kinase Complex\")) -> kin(p(PFM:\"Akt Family\"))" .
}
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 examined the effect of blockade of type 1 IGF tyrosine kinase receptor (IGF-IR) in a murine model of bleomycin-induced lung injury and fibrosis. Mice were treated with a monoclonal antibody against the IGF-I receptor (A12) or vehicle after intratracheal bleomycin instillation. MEASUREMENTS AND MAIN RESULTS: Mice treated with A12 antibody had significantly improved survival after bleomycin injury compared with control mice. Both groups of mice had a similar degree of fibrosis on days 7 and 14, but by Day 28 the A12-treated group had significantly less fibrosis. Delayed treatment with A12 also resulted in decreased fibrosis. A12-treated mice had significantly decreased apoptotic cells on Day 28 compared with control mice. We confirmed that A12 treatment induced mouse lung fibroblast apoptosis in vitro. In addition, IGF-I increased lung fibroblast migration. The primary pathway activated by IGF-I in lung fibroblasts was the insulin receptor substrate-2/phosphatidylinositol 3-kinase/Akt axis.";
prov:wasQuotedFrom pubmed:19011156 .
sub:_6 rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:19011156;
prov:wasDerivedFrom beldoc:, sub:_5 .
}
sub:pubinfo {
this: dcterms:created "2014-07-03T14:30:53.948+02:00"^^xsd:dateTime;
pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}