@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 go: . @prefix Protein: . @prefix mgi: . @prefix geneProductOf: . @prefix hasAgent: . @prefix obo: . @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 hasAgent: sub:_2; a go:0003824 . sub:_2 geneProductOf: mgi:102845; a Protein: . sub:_3 occursIn: obo:UBERON_0004535, species:10090; rdf:object go:0043114; rdf:predicate belv:increases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "cat(p(MGI:Bdkrb2)) -> bp(GOBP:\"regulation of vascular permeability\")" . } 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 "20131211" . sub:_4 prov:value "# Pubmed:gene: Increased vascular permeability in C1 inhibitor-deficient mice mediated by the bradykinin type 2 receptor. This increased vascular permeability was reversed by treatment with intravenous human C1INH, with a Kunitz domain plasma kallikrein inhibitor (DX88), and with a bradykinin type 2 receptor (Bk2R) antagonist (Hoe140). In addition, treatment of the C1INH-deficient mice with an angiotensin-converting enzyme inhibitor (captopril) increased the vascular permeability. Bradykinin is a small peptide vasodilator formed in blood and tissue fluids by cleavage of alpha2-globulins. It causes both arteriolar dilation and increased capillary permeability"; prov:wasQuotedFrom pubmed:11956243 . sub:_5 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:11956243; prov:wasDerivedFrom beldoc:, sub:_4 . } sub:pubinfo { this: dct:created "2014-07-03T14:31:48.465+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }