@prefix dcterms: <http://purl.org/dc/terms/> .
@prefix this: <http://www.tkuhn.ch/bel2nanopub/RAjxt_BxQtEDOWqTLoZ1BdnM7LLWJtT07MK8UJaKWlOuM> .
@prefix sub: <http://www.tkuhn.ch/bel2nanopub/RAjxt_BxQtEDOWqTLoZ1BdnM7LLWJtT07MK8UJaKWlOuM#> .
@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 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 scomp: <http://resource.belframework.org/belframework/20131211/namespace/selventa-named-complexes/> .
@prefix ProteinComplex: <http://amigo.geneontology.org/amigo/term/GO:0043234> .
@prefix hasAgent: <http://semanticscience.org/resource/SIO_000139> .
@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 species: <http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=> .
@prefix occursIn: <http://purl.obolibrary.org/obo/BFO_0000066> .
@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 {
  scomp:AP-1%20Complex a ProteinComplex: .
  
  sub:_1 hasAgent: scomp:AP-1%20Complex;
    a go:0042789 .
  
  sub:_2 geneProductOf: mgi:1314884;
    a RNA: .
  
  sub:_3 occursIn: species:10090;
    rdf:object sub:_2;
    rdf:predicate belv:increases;
    rdf:subject sub:_1;
    a rdf:Statement .
  
  sub:assertion rdfs:label "tscript(complex(SCOMP:\"AP-1 Complex\")) -> r(MGI:Tnfrsf1a)" .
}

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 "In human circulating monocytes, inhibition of PDE4 by rolipram markedly suppresses TNF- synthesis and release in response to LPS; ... LPS stimulation of macrophages induces a large increase in TNF- mRNA by increasing gene transcription via activation of the transcriptional factors NF-B (13-15), c-jun, and c-fos (16). ... A study investigating the control of TNF- synthesis by using reporter constructs has demonstrated that this AU-rich element and the flanking sequences are sufficient to mediate a more than 200-fold increase in the LPS-dependent synthesis of the reporter protein. This element is involved in both the control of mRNA degradation and its translation This increase is not due to a change in cytoplasmic mRNA concentration but rather to a reversal of the translation repression in response to LPS ...The consequent increase in PDE activity leads to a decrease in cAMP, thus removing the cAMP constraint and allowing a full induction of TNF- mRNA and protein synthesis. The induction of PDE4B should then be viewed as a positive feedback loop that contributes to a full activation of the cytokine responses.";
    prov:wasQuotedFrom pubmed:12032334 .
  
  sub:_5 rdfs:label "Selventa" .
  
  sub:assertion prov:hadPrimarySource pubmed:12032334;
    prov:wasDerivedFrom beldoc:, sub:_4 .
}

sub:pubinfo {
  this: dcterms:created "2014-07-03T14:31:49.579+02:00"^^xsd:dateTime;
    pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}