@prefix this: <http://www.tkuhn.ch/bel2nanopub/RAf5Gjgek57K4nGLzYOImM0IInXqRxjJtomL9ZCMzzTuA> .
@prefix sub: <http://www.tkuhn.ch/bel2nanopub/RAf5Gjgek57K4nGLzYOImM0IInXqRxjJtomL9ZCMzzTuA#> .
@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 schem: <http://resource.belframework.org/belframework/1.0/namespace/selventa-legacy-chemical-names/> .
@prefix go: <http://amigo.geneontology.org/amigo/term/GO:> .
@prefix Protein: <http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI_36080> .
@prefix hgnc: <http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=> .
@prefix geneProductOf: <http://purl.obolibrary.org/obo/RO_0002204> .
@prefix hasAgent: <http://semanticscience.org/resource/SIO_000139> .
@prefix atcc: <http://www.lgcstandards-atcc.org/Products/All/> .
@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 hasAgent: sub:_2;
    a go:0042789 .
  
  sub:_2 geneProductOf: hgnc:3467;
    a Protein: .
  
  sub:_3 occursIn: atcc:CCL-2.aspx, species:9606;
    rdf:object sub:_1;
    rdf:predicate belv:increases;
    rdf:subject schem:cyclic%20AMP;
    a rdf:Statement .
  
  sub:assertion rdfs:label "a(SCHEM:\"cyclic AMP\") -> tscript(p(HGNC:ESR1))" .
}

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 "1.4" .
  
  sub:_4 prov:value "Cotransfection of the reporter genes with truncated versions of the ER shows that the two non-ligand activators of ER require different regions of the receptor to produce their effects on transcription. EGF acts primarily by means of transactivation domain AF-1, whereas cAMP acts via transactivation domain AF-2 of the ER. A point mutation that removes a major site of inducible phosphorylation within the AF-1 domain of the ER abolishes the response to EGF, but the response to estradiol and cAMP is retained. Specific inhibition of cAMP-activated protein kinase (protein kinase A) prevents the response to elevated cAMP but does not affect EGF or estradiol responses. Overexpression of the protein kinase A catalytic subunit in HeLa cells results in an amplified response to estradiol, similar to that induced by cholera toxin with 3-isobutyl-1-methyl-xanthine. Comparable experiments performed using COS-1 cells produce similar results but also reveal cell type- and promoter-specific aspects of the activation mechanisms. Apparently, the ER may be activated by three different signal molecules, estradiol, EGF, and cAMP, each using a mechanism that is distinguishable from that of the others.";
    prov:wasQuotedFrom pubmed:9178752 .
  
  sub:_5 rdfs:label "Selventa" .
  
  sub:assertion prov:hadPrimarySource pubmed:9178752;
    prov:wasDerivedFrom beldoc:, sub:_4 .
}

sub:pubinfo {
  this: dct:created "2014-07-03T14:30:58.399+02:00"^^xsd:dateTime;
    pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}