@prefix this: <http://www.tkuhn.ch/bel2nanopub/RATHkJDbMZEvxAS9kiCxFEO1qdiiRu_FNCTEmaFiLUS1M> .
@prefix sub: <http://www.tkuhn.ch/bel2nanopub/RATHkJDbMZEvxAS9kiCxFEO1qdiiRu_FNCTEmaFiLUS1M#> .
@prefix beldoc: <http://resource.belframework.org/belframework/1.0/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 Protein: <http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI_36080> .
@prefix mgi: <http://www.informatics.jax.org/marker/MGI:> .
@prefix geneProductOf: <http://purl.obolibrary.org/obo/RO_0002204> .
@prefix schem: <http://resource.belframework.org/belframework/1.0/namespace/selventa-legacy-chemical-names/> .
@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 {
  sub:_1 geneProductOf: mgi:96543;
    a Protein: .
  
  sub:_2 occursIn: species:10090;
    rdf:object schem:Serum%20Glucagon;
    rdf:predicate belv:increases;
    rdf:subject sub:_1;
    a rdf:Statement .
  
  sub:assertion rdfs:label "p(MGI:Il1b) -> a(SCHEM:\"Serum Glucagon\")" .
}

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 "IL-1 was reported to be involved in the feeding suppression caused by leptin, which is released from adipocytes and suppresses food intake through actions in the hypothalamus. IL-1 promotes the release of corticotropin releasing factor (CRF; references 18, 19), melanocortins, and other neuropeptides (4). CRF suppresses feeding behavior when administered intracerebroventricularly. IL-1B selectively destroys the insulin-producing B cells, but not the {alpha} cells, in vitro. This cytotoxic effect of IL-1 is suggested to be mediated by the induction of inducible nitric oxide synthase or prostaglandins On the other hand, it was reported that IL-1 acts as a hypoglycemic agent not only in normal animals but also in alloxan-induced diabetic and genetically diabetic mice (32) and increases insulin and glucagon levels, suggesting that IL-1 has antidiabetic effects (33)";
    prov:wasQuotedFrom pubmed:12975454 .
  
  sub:_4 rdfs:label "Selventa" .
  
  sub:assertion prov:hadPrimarySource pubmed:12975454;
    prov:wasDerivedFrom beldoc:, sub:_3 .
}

sub:pubinfo {
  this: dct:created "2014-07-03T14:30:16.605+02:00"^^xsd:dateTime;
    pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}