Figure 7
Figure 7. The p53 pathway is rarely dysregulated in v-abl plasmacytomas. (A) Western blot analysis of primary v-abl, mcl-1/v-abl, and bim−/−v-abl tumor tissue and Eμ-myc tumor 48 (positive control for mutant p53). (B) p53 activation in v-abl plasmacytoma cells following exposure to the Mdm-2 inhibitor Nutlin 3a. v-abl tumor cells (CD138+) isolated by flow cytometry from ascites in transplanted mice were cultured with 50 µM Q-VD-OPh alone (−) or in combination with 10 µM Nutlin 3a (+) for 16 h and then harvested for western blot analysis. Controls were Eµ-myc cell lines 22 (mutant for p53) and 45 (WT for p53). MW markers are indicated (kDa).

The p53 pathway is rarely dysregulated in v-abl plasmacytomas. (A) Western blot analysis of primary v-abl, mcl-1/v-abl, and bim−/−v-abl tumor tissue and Eμ-myc tumor 48 (positive control for mutant p53). (B) p53 activation in v-abl plasmacytoma cells following exposure to the Mdm-2 inhibitor Nutlin 3a. v-abl tumor cells (CD138+) isolated by flow cytometry from ascites in transplanted mice were cultured with 50 µM Q-VD-OPh alone (−) or in combination with 10 µM Nutlin 3a (+) for 16 h and then harvested for western blot analysis. Controls were Eµ-myc cell lines 22 (mutant for p53) and 45 (WT for p53). MW markers are indicated (kDa).

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