Expression data upon K-Ras elimination in DU, DU RRAS2 G23V and DU PI3KCAAX cells

The expression of an oncogenic version (G23V mutant) of R-Ras2/TC21 can fully compensate for the loss of the three classical Ras proteins in MEFs. This process involves the inhibition of the antiproliferative p53–p21Cip1 retinoblastoma axis known to cause the morphological and proliferative defects found in Ras-deficient MEFs. Unlike the case of normal MEFs, the inhibition of this antiproliferative pathway by R-Ras2G23V in Ras-deficient cells is mediated by PI3Ka–dependent rather than ERK-dependent signaling inputs. We used microarrays to detail the global programme of gene expression underlying this compensation process. We used triplicates of DU control, RRAS2G23V, and PI3KCAAX cells with and without 4-OHT.