Complementary functions of A1 and pim-1 in restoring the transforming capacity of the BCR/ABLΔΔ mutant.

32DHN control cells (Figure 2) and 32DHN-A1+pim-1 (overexpressing A1 and pim-1) cells were infected with BCR/ABL WT-IRES-GFP or BCR/ABLΔΔ-IRES-GFP retroviruses, respectively. GFP⁺cells were analyzed for (A) expression of BCR/ABL, A1 and pim-1 proteins, (B) apoptosis in IL-3–deficient medium, and (C) growth factor–independent proliferation (details are given in legends to Figures 2 and 3). Results represent 3 experiments.