@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 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: hgnc:11850; a Protein: . sub:_3 occursIn: obo:CL_0000145, species:9606; rdf:object sub:_1; rdf:predicate belv:increases; rdf:subject ; a rdf:Statement . sub:assertion rdfs:label "path(SDIS:\"bacterial infection\") -> cat(p(HGNC:TLR4))" . } 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 "from full text - We previously showed that TL1A is induced by the Fc?R signaling pathway [45]. Recently, the potential interaction of TL1A in microbial-host interaction was illustrated by a report showing microbial organisms can induce TL1A in APCs [46]. Microbial-activated TL1A was in part mediated by TLR 1, 2, 4, and 9 signaling pathways and dependent on downstream p38 MAP kinase and NF-kappaB activation (Fig. 1) [46]. Negative regulators of the TL1A signaling pathway also exist and may serve to maintain gut immune homeostasis. Our group showed that TLR8 or TLR7/8 ligand (R848) can inhibit TL1A production in a dose dependent manner [47•]."; prov:wasQuotedFrom pubmed:19903423 . sub:_5 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:19903423; prov:wasDerivedFrom beldoc:, sub:_4 . } sub:pubinfo { this: dct:created "2014-07-03T14:33:37.516+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }