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 "To test if activation of HRas or NRas by eNOS is required for pancreatic tumour growth, HRas or NRas were knocked down by shRNA in CFPac-1 and/or MIAPaCa-2 cells and complemented with an HRas or NRas that was engineered to be resistant to RNAi (HRasR, NRasR) in the wild-type or C118S mutant configuration. Resultant cells were then assayed for tumour growth in mice. Positive control, scramble-treated CFPac-1 and/or MIAPaCa-2 cells readily formed tumours in mice, whereas this growth was reduced when endogenous HRas, and to a lesser degree NRas, was knocked down. This loss of tumour growth was rescued by expressing the appropriate wild-type HRas or NRas, but not the C118S nitrosylation mutants (Fig. 4e, f and Supplementary Figs 11–13" ;
    prov:wasQuotedFrom pubmed:18344980 .
  sub:_5 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:18344980 ;
    prov:wasDerivedFrom beldoc: , sub:_4 .
}