Fig. 4

R-RAS2 controls PI3K/Akt, ERK/MAPK and mTORC1 pathway activation in murine RRAS2-overexpressing breast cancer cells. a, Cartoon illustrating RAS/ERK/MAPK, PI3K/Akt and mTORC1 pathway activation by Receptor Tyrosine Kinases (RTKs) like EphaA2, EGFR or HER2, and by amino acid transporters like the CD98hc/CD98lc(LAT1) complex, and by CD44. The positions of some relevant phosphorylated residues are indicated, as well as the putative position of R-RAS2 downstream of the RTKs, CD44 and CD98. b, Western blot analysis of signaling pathway activity based on the phosphorylation of key residues in the elements indicated. Post-nuclear cell lysates of wild type CBM-MBC21 cells and a shRNA-generated RRAS2 knockdown of that cell line were analyzed in the blots. c, Summary of the results generated by Western blot. The inhibitory effect of R-RAS2 depletion is indicated by the number of arrows pointing downwards