@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 Protein: . @prefix mgi: . @prefix geneProductOf: . @prefix go: . @prefix species: . @prefix occursIn: . @prefix mesh: . @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: mgi:98737; a Protein: . sub:_2 occursIn: mesh:D008264, species:10090; rdf:object go:0001525; rdf:predicate belv:decreases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "p(MGI:Thbs1) -| 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:_4; pav:version "1.4" . sub:_3 prov:value "\\\"The antiangiogenic effect of thrombospondin-2 is mediated by CD36 and modulated by histidine-rich glycoprotein.\\\" We have previously shown that the antiangiogenic activity of TSP-1 is mediated by the interaction of the type I repeats (TSR) with the receptor CD36, although other domains of TSP-1 have also been implicated. We now show that the antiangiogenic activity of TSP-2, which contains three TSRs but, unlike TSP-1, lacks the capacity to activate TGF-beta, is similarly dependent on CD36. sing the corneal pocket assay we found that TSP-2 did not inhibit bFGF-induced angiogenesis in CD36 null mice."; prov:wasQuotedFrom pubmed:15748999 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:15748999; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:33.273+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }