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Matches in Nanopublications for { ?s ?p "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" ?g. }

• _4 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" provenance.
• _4 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" provenance.