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 .
}