@prefix this: <http://www.tkuhn.ch/bel2nanopub/RAwVc0kBpA7jvl8kPJGAtQA1VjwOEKTArv7E1YtrUqres> .
@prefix sub: <http://www.tkuhn.ch/bel2nanopub/RAwVc0kBpA7jvl8kPJGAtQA1VjwOEKTArv7E1YtrUqres#> .
@prefix beldoc: <http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel> .
@prefix rdfs: <http://www.w3.org/2000/01/rdf-schema#> .
@prefix rdf: <http://www.w3.org/1999/02/22-rdf-syntax-ns#> .
@prefix xsd: <http://www.w3.org/2001/XMLSchema#> .
@prefix dct: <http://purl.org/dc/terms/> .
@prefix dce: <http://purl.org/dc/elements/1.1/> .
@prefix pav: <http://purl.org/pav/> .
@prefix np: <http://www.nanopub.org/nschema#> .
@prefix belv: <http://www.selventa.com/vocabulary/> .
@prefix prov: <http://www.w3.org/ns/prov#> .
@prefix go: <http://amigo.geneontology.org/amigo/term/GO:> .
@prefix RNA: <http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI_33697> .
@prefix mgi: <http://www.informatics.jax.org/marker/MGI:> .
@prefix geneProductOf: <http://purl.obolibrary.org/obo/RO_0002204> .
@prefix obo: <http://purl.obolibrary.org/obo/> .
@prefix occursIn: <http://purl.obolibrary.org/obo/BFO_0000066> .
@prefix species: <http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=> .
@prefix pubmed: <http://www.ncbi.nlm.nih.gov/pubmed/> .
@prefix orcid: <http://orcid.org/> .

sub:Head {
  this: np:hasAssertion sub:assertion;
    np:hasProvenance sub:provenance;
    np:hasPublicationInfo sub:pubinfo;
    a np:Nanopublication .
}

sub:assertion {
  sub:_1 geneProductOf: mgi:109603;
    a RNA: .
  
  sub:_2 occursIn: obo:CL_0000235, species:10090;
    rdf:object sub:_1;
    rdf:predicate belv:decreases;
    rdf:subject go:0006954;
    a rdf:Statement .
  
  sub:assertion rdfs:label "bp(GOBP:\"inflammatory response\") -| r(MGI:Cmklr1)" .
}

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 "20131211" .
  
  sub:_3 prov:value "In general, proinflammatory cytokines and TLR ligands suppressed mCMKLR1 expression (Fig. 5, upper panel). We observed the following hierarchy in mCMKLR1 suppression by TLR ligands: LPS O polyI:C O CpG. The proinflammatory cytokines IFN-g and TNF-a caused modest mCMKLR1 suppression as well, which was enhanced by coincubation with LPS. Interestingly, the immune-suppressive cytokine TGF-b had the opposite effect on receptor expression: overnight treatment with either TGF-b1 or TGF-b2 resulted in mCMKLR1 upregulation";
    prov:wasQuotedFrom pubmed:16863918 .
  
  sub:_4 rdfs:label "Selventa" .
  
  sub:assertion prov:hadPrimarySource pubmed:16863918;
    prov:wasDerivedFrom beldoc:, sub:_3 .
}

sub:pubinfo {
  this: dct:created "2014-07-03T14:33:02.311+02:00"^^xsd:dateTime;
    pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}