@prefix this: . @prefix sub: . @prefix beldoc: . @prefix rdfs: . @prefix rdf: . @prefix xsd: . @prefix dct: . @prefix dce: . @prefix pav: . @prefix np: . @prefix belv: . @prefix prov: . @prefix schem: . @prefix go: . @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 { sub:_1 occursIn: mesh:D004730, species:9606; rdf:object go:0008283; rdf:predicate belv:decreases; rdf:subject schem:Angiostatin; a rdf:Statement . sub:assertion rdfs:label "a(SCHEM:Angiostatin) -| bp(GO:\"cell proliferation\")" . } 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:_3; pav:version "1.4" . sub:_2 prov:value "Also members of the selectin family, in particular P-selectin and E-selectin, which promotes adhesion of leukocytes to cytokine-activated vascular endothelium, have been shown to play a role in angiogenesis (134). E-selectin was found to induce endothelial migration and tube formation in vitro and angiogenesis in vivo (167). However, little is known about the mechanism of action of these molecules and mice deficient in both E-selectin and P-selectin are viable and fertile (139)."; prov:wasQuotedFrom pubmed:11172729 . sub:_3 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:11172729; prov:wasDerivedFrom beldoc:, sub:_2 . } sub:pubinfo { this: dct:created "2014-07-03T14:29:54.167+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }