. . . . . . . . . . . . . . "gtp(p(HGNC:HRAS)) -> path(SDIS:\"tumor growth\")" . "Approximately 61,000 statements." . "Copyright (c) 2011-2012, Selventa. All rights reserved." . "BEL Framework Large Corpus Document" . . "20131211" . "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" . . "Selventa" . . . . "2014-07-03T14:33:18.638+02:00"^^ . . .