@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 hgnc: . @prefix geneProductOf: . @prefix hasAgent: . @prefix species: . @prefix occursIn: . @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: hgnc:7562; a Protein: . sub:_3 hasAgent: sub:_4; a go:0016301 . sub:_4 geneProductOf: hgnc:6112; a Protein: . sub:_5 occursIn: species:9606; rdf:object sub:_3; rdf:predicate belv:increases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "cat(p(HGNC:MYD88)) -> kin(p(HGNC:IRAK1))" . } 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:_7; pav:version "1.4" . sub:_6 prov:value "Tollip is present in a complex with IRAK, and that recruitment of Tollip-IRAK complexes to the activated receptor complex occurs through association of Tollip with IL-1RAcP. Co-recruited MyD88 then triggers IRAK autophosphorylation, which in turn leads to rapid dissociation of IRAK from Tollip (and IL-1Rs). As overexpression of Tollip results in impaired NF-kappaB activation, we conclude that Tollip is an important constituent of the IL-1R signalling pathway."; prov:wasQuotedFrom pubmed:10854325 . sub:_7 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:10854325; prov:wasDerivedFrom beldoc:, sub:_6 . } sub:pubinfo { this: dct:created "2014-07-03T14:29:51.314+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }