@prefix dc: . @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 pfh: . @prefix geneProductOf: . @prefix go: . @prefix hasAgent: . @prefix mesh: . @prefix occursIn: . @prefix hasAnnotation: . @prefix atcc: . @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: pfh:VEGF%20Family; a Protein: . sub:_2 hasAgent: sub:_3; a go:0016301 . sub:_3 geneProductOf: pfh:AKT%20Family; a Protein: . sub:_4 rdf:object sub:_2; rdf:predicate belv:increases; rdf:subject sub:_1; a rdf:Statement . sub:_5 occursIn: mesh:D002478, mesh:D014471, mesh:D042783, atcc:CRL-1730.aspx; hasAnnotation: sub:_6; rdf:object sub:_4; rdf:predicate belv:decreases; rdf:subject schem:Smoke%20extract%2C%20cigarette; a rdf:Statement . sub:_6 dc:subject "TextLocation"; rdf:value "Results" . sub:assertion rdfs:label "a(SCHEM:\"Smoke extract, cigarette\") -| (p(PFH:\"VEGF Family\") -> kin(p(PFH:\"AKT Family\")))", "p(PFH:\"VEGF Family\") -> kin(p(PFH:\"AKT Family\"))" . } sub:provenance { beldoc: dce:description "Approximately 2000 hand curated statements drawn from 57 PubMeds."; dce:rights "Copyright (c) 2011-2012, Selventa. All Rights Reserved."; dce:title "BEL Framework Small Corpus Document"; dc:license "Creative Commons Attribution-Non-Commercial-ShareAlike 3.0 Unported License"; pav:authoredBy sub:_8; pav:version "1.6" . sub:_7 prov:value """Because NO is an essential mediator of endothelial cell migration and VEGF-induced angiogenesis, we investigated the effect of CSE exposure on VEGF-dependent Akt/eNOS/NO pathway. VEGF-stimulated HUVECs exposed to CSE show a dose-dependent inhibition of phosphorylated Akt and eNOS (Fig. 4A). Importantly, the activation of Akt and eNOS by VEGF can be rescued following treatment with the antioxidants NAC and vitamin C (Fig. 4B). Similarly, we found that the induction of NO by VEGF in endothelial cell cultures was severely compromised in the presence of CSE, but that NO levels could be normalized with antioxidants (Fig. 4C). Globally, these data suggest that ROS are involved in the impairment of VEGF-induced Akt/eNOS/NO pathway by CSE."""; prov:wasQuotedFrom pubmed:16806264 . sub:_8 rdfs:comment "support@belframework.org"; rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:16806264; prov:wasDerivedFrom beldoc:, sub:_7 . } sub:pubinfo { this: dc:created "2014-07-03T14:29:31.651+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }