@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 chebi: . @prefix Protein: . @prefix hgnc: . @prefix geneProductOf: . @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 geneProductOf: hgnc:6112; a Protein: . sub:_2 occursIn: species:9606; rdf:object sub:_1; rdf:predicate belv:decreases; rdf:subject chebi:6494; a rdf:Statement . sub:assertion rdfs:label "a(CHEBI:lipopolysaccharide) -| 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:_4; pav:version "1.4" . sub:_3 prov:value "Rapid degradation of IRAK, occurring within 30 min of exposure to agonist, was shown to signal through CD14/TLR4 and was regulated by phosphatidylinositol 3-kinase. A second delayed wave of IRAK degradation occurred 2 h after exposure to LPS and was mediated by CR3 independently of phosphatidylinositol 3-kinase. Thus, multiple independent mechanisms have evolved to regulate IRAK degradation, likely reflecting the importance of limiting cellular responses to LPS."; prov:wasQuotedFrom pubmed:15069085 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:15069085; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:22.435+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }