@prefix this: <http://www.tkuhn.ch/bel2nanopub/RAXs9KTpZ2ogIyOvfWAohipGt-eIUQyR91Gt8tdY0rLac> .
@prefix sub: <http://www.tkuhn.ch/bel2nanopub/RAXs9KTpZ2ogIyOvfWAohipGt-eIUQyR91Gt8tdY0rLac#> .
@prefix beldoc: <http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel> .
@prefix rdfs: <http://www.w3.org/2000/01/rdf-schema#> .
@prefix rdf: <http://www.w3.org/1999/02/22-rdf-syntax-ns#> .
@prefix xsd: <http://www.w3.org/2001/XMLSchema#> .
@prefix dct: <http://purl.org/dc/terms/> .
@prefix dce: <http://purl.org/dc/elements/1.1/> .
@prefix pav: <http://purl.org/pav/> .
@prefix np: <http://www.nanopub.org/nschema#> .
@prefix belv: <http://www.selventa.com/vocabulary/> .
@prefix prov: <http://www.w3.org/ns/prov#> .
@prefix go: <http://amigo.geneontology.org/amigo/term/GO:> .
@prefix Protein: <http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI_36080> .
@prefix hgnc: <http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=> .
@prefix geneProductOf: <http://purl.obolibrary.org/obo/RO_0002204> .
@prefix hasAgent: <http://semanticscience.org/resource/SIO_000139> .
@prefix species: <http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=> .
@prefix occursIn: <http://purl.obolibrary.org/obo/BFO_0000066> .
@prefix mesh: <http://purl.bioontology.org/ontology/MSH/> .
@prefix pubmed: <http://www.ncbi.nlm.nih.gov/pubmed/> .
@prefix orcid: <http://orcid.org/> .

sub:Head {
  this: np:hasAssertion sub:assertion;
    np:hasProvenance sub:provenance;
    np:hasPublicationInfo sub:pubinfo;
    a np:Nanopublication .
}

sub:assertion {
  sub:_1 hasAgent: sub:_2;
    a go:0016301 .
  
  sub:_2 geneProductOf: hgnc:3688;
    a Protein: .
  
  sub:_3 occursIn: mesh:D004730, mesh:D042783, species:9606;
    rdf:object go:0001525;
    rdf:predicate belv:increases;
    rdf:subject sub:_1;
    a rdf:Statement .
  
  sub:assertion rdfs:label "kin(p(HGNC:FGFR1)) -> bp(GO:angiogenesis)" .
}

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:_5;
    pav:version "1.4" .
  
  sub:_4 prov:value "Several experimental evidences point to the possibility that FGF2 induces neovascularization indirectly by activation of the VEGF/ VEGFR system. Indeed: (i) VEGFR-2 antagonists inhibit both VEGF and FGF2-induced angiogenesis in vitro and in vivo [98]; (ii) expression of dominant-negative FGFR1 or FGFR2 in glioma cells results in a decrease in tumor vascularization paralleled by VEGF down-regulation [99]; (iii) both endogenous and exogenous FGF2 modulate VEGF expression in endothelial cells [82]; (iv) in the mouse cornea, the quiescent endothelium of vessels of the limbus express both VEGF mRNA and protein only after FGF2 treatment. In the same model, systemic administration of anti-VEGF-A neutralizing antibodies dramatically reduces FGF2-induced vascularization [82]; (v) VEGFR-1-blocking antibodies or the expression of a dominant-negative VEGFR-1 result in a significant reduction of FGF2-induced cell extensions and capillary morphogenesis [56]; (vi) FGF2 upregulates the expression of both FGFRs and VEGFRs in endothelial cells [100].";
    prov:wasQuotedFrom pubmed:15863032 .
  
  sub:_5 rdfs:label "Selventa" .
  
  sub:assertion prov:hadPrimarySource pubmed:15863032;
    prov:wasDerivedFrom beldoc:, sub:_4 .
}

sub:pubinfo {
  this: dct:created "2014-07-03T14:30:34.811+02:00"^^xsd:dateTime;
    pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}