@prefix this: <http://www.tkuhn.ch/bel2nanopub/RAbT8Y4XMBII-vQSwlmjfrj9DY1ycguV_nzZ7CGUbMCDE> .
@prefix sub: <http://www.tkuhn.ch/bel2nanopub/RAbT8Y4XMBII-vQSwlmjfrj9DY1ycguV_nzZ7CGUbMCDE#> .
@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 hgnc: <http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=> .
@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 {
  sub:_1 geneProductOf: hgnc:11766;
    a Protein: .
  
  sub:_2 geneProductOf: hgnc:3236;
    a Protein: .
  
  sub:_3 occursIn: species:9606;
    rdf:object sub:_2;
    rdf:predicate belv:increases;
    rdf:subject sub:_1;
    a rdf:Statement .
  
  sub:assertion rdfs:label "p(HGNC:TGFB1) -> p(HGNC:EGFR)" .
}

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 "Although the growth-inhibitory effect of TGF-B is believed to be mediated by the Smad dependent TGF-B signaling pathway, there have been reports of TGF-B mediated inhibition of proliferation in Smad4 null cells.22 Proposed alternative mechanisms for resistance to TGF-B include decreased expression of TBRI,34 TBRII,35 or TBRIII36 on the cell surface; increased expression of the inhibitory Smad, Smad7; repression of TGF-B signaling by a variety of oncoproteins including p53,38 Myc,39 E1A,40 Ras,41 Ski/ SnoN,42,43 and Evi-1 44; reduced expression or inactivation of tumor suppressors that directly regulate the TGF-B signaling pathway including Menin,45 Disabled-2 ,46 and RUNX3; and activation of other signaling pathways includings protein kinase C (PKC). TGF-B is able to increase the production of mitogenic growth factors, including platelet-derived growth factor,51 fibroblast growth factor,52 TGF-B,53 and connective tissue growth factor,54 and to increase expression of the platelet derived growth factor receptor,55 and the epithelial growth factor receptor.56 In addition, TGF-B can activate Smad independent pathways, including the Ras/Raf/MAPK pathway,20-22,57,58 which often mediates the proliferative signal of growth factors. Indeed, it is in conjunction with oncogenic forms of Ras (Ha-Ras or Ki-Ras), that TGF-B drives Smad-independent proliferation of human colon and prostate cancer cells.3,49";
    prov:wasQuotedFrom pubmed:15774796 .
  
  sub:_5 rdfs:label "Selventa" .
  
  sub:assertion prov:hadPrimarySource pubmed:15774796;
    prov:wasDerivedFrom beldoc:, sub:_4 .
}

sub:pubinfo {
  this: dct:created "2014-07-03T14:30:33.480+02:00"^^xsd:dateTime;
    pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}