Fig. 5: Oncogenic NRAS mutants mediate differential MAPK activation via a RAF-dependent mechanism.

Representative immunoblots of AKT and ERK activation in homozygous MEF cell lines treated with shRNAs targeting Nras, Hras and Kras, or Sos1 (a) or Araf, Braf or Craf (b). Dot plot data are presented as mean values +/− SD where each dot represents one biological replicate. For a the following biologically independent replicates per genotype were examined over five independent experiments (eGFP arm: Q = 5, P = 5, R = 5; NRAS arm: Q = 3, P = 3, R = 3; H/KRAS arm: Q = 3, P = 4, R = 3; SOS1 arm: Q = 5, P = 5, R = 5). For b the following biologically independent replicates per genotype were examined over 8 independent experiments (eGFP arm: Q = 8, P = 8, R = 8; ARAF arm: Q = 6, P = 6, R = 6; BRAF arm: Q = 7, P = 7, R = 6; CRAF arm: Q = 7, P = 7, R = 6). Adjusted p-values were generated using a one-way ANOVA with a Tukey’s multiple comparisons test. Statistics denoted in the figure indicate significant differences between shRNA-treated NRAS mutant MEFs and their respective eGFP control. ** p < 0.01, † p < 0.001. A complete list of adjusted p-values can be found in Supplementary Table 4a, b. Source data are provided as a Source Data file.