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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RApUgA4-zbTeE5fpLpxJp4B-KUJrd30__U3vCyIaSixEY#_5 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RApUgA4-zbTeE5fpLpxJp4B-KUJrd30__U3vCyIaSixEY#_4 http://www.w3.org/ns/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. 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