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sub:Head {
  this: np:hasAssertion sub:assertion ;
    np:hasProvenance sub:provenance ;
    np:hasPublicationInfo sub:pubinfo ;
    a np:Nanopublication .
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sub:assertion {
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    rdf:predicate belv:increases ;
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  sub:_3 dct:subject "TextLocation" ;
    rdf:value "Results" .
  sub:assertion rdfs:label "p(HGNC:MAP2K7) -> path(MESHD:\"Carcinoma, Squamous Cell\")" .
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sub:provenance {
  beldoc: dce:description "Approximately 2000 hand curated statements drawn from 57 PubMeds." ;
    dce:rights "Copyright (c) 2011-2012, Selventa. All Rights Reserved." ;
    dce:title "BEL Framework Small Corpus Document" ;
    dct:license "Creative Commons Attribution-Non-Commercial-ShareAlike 3.0 Unported License" ;
    pav:authoredBy sub:_5 ;
    pav:version "1.6" .
  sub:_4 prov:value """We next asked whether components of the JNK cascade could directly promote human epidermal
neoplasia. We expressed either active MKK7 or c-Jun in primary keratinocytes
and examined their capacity to promote tumorigenesis in combination with
Ras in the absence of IκBα. First, we confirmed induction of AP1-dependent gene
reporter activity by MKK7 in vitro (Supplementary Fig. S4). Surface skin grafts
were then regenerated with primary keratinocytes expressing MKK7 and Ras; these
developed into clinical tumors resembling SCC (Fig. 3A). Dermal invasion, one of
the hallmarks of spontaneous human SCC, is apparent in tumors induced by MKK7 and
Ras as revealed by both histologic appearance and BMZ disruption (Fig. 3B–C).
MKK7 and Ras-induced neoplasia depends on intact AP1 function as concurrent expression
of DNc-Jun prevents tumorigenesis (Fig. 3A–C).""" ;
    prov:wasQuotedFrom pubmed:17440097 .
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  sub:assertion prov:hadPrimarySource pubmed:17440097 ;
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sub:pubinfo {
  this: dct:created "2014-07-03T14:29:32.894+02:00"^^xsd:dateTime ;
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}