@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 hgnc: . @prefix geneProductOf: . @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 geneProductOf: hgnc:11892; a Protein: . sub:_2 occursIn: mesh:D008168, species:9606; rdf:object go:0043114; rdf:predicate belv:increases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "p(HGNC:TNF) -> bp(GO:\"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:_4; pav:version "1.4" . sub:_3 prov:value "possibly through extracellular signal-regulated kinase (ERK)-catalyzed caldesmon phosphorylation and subsequent alteration of actomyosin cross bridging. Likewise, the cytokine TNF- through its receptor (TNF-R) appears to mediate cytoskeletal rearrangement and eventual barrier dysfunction through a PKC-dependent pathway. Although TNF- produces an increase in MLC phosphorylation, this effect does not appear to contribute to the subsequent increase in EC permeability. "; prov:wasQuotedFrom pubmed:11568129 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:11568129; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:29:58.274+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }