![Figure 5. ABL1 promotes apoptosis in BCR-ABL1 leukemia cells in response to genotoxic agents. (A) Results represent mean percentage of clonogenic activity ± SD of BCR-ABL1 Abl1−/− (●) and BCR-ABL1 Abl1+/+ (○) leukemia cells after treatment with indicated DNA damage-inducing agents in the presence (top row) or absence (bottom row) of SCF + IL-3; *P < .05. (B) Western blot analysis of p73, p53, phospho-serine 15 of p53 (phospho-p53) and activated caspase 3 in BCR-ABL1 Abl1−/− [−/−], BCR-ABL1 Abl1+/+ [+/+], and BCR-ABL1/YFP-ABL1 Abl1−/− [−/−(+)] leukemia cells treated with cisplatin (0.25 μg/mL); tubulin served as loading control. (C) Statistically significant (FDR < 0.05) fold changes (>2.0) of expression of indicated genes in BCR-ABL1 Abl1−/− vs BCR-ABL1 Abl1+/+ leukemia cells maintained with SCF + IL-3.](https://ash.silverchair-cdn.com/ash/content_public/journal/blood/127/17/10.1182_blood-2015-11-681171/4/2131f5.jpeg?Expires=1735826205&Signature=JVPafTcnmGLx4-Gb5ql4GoRJJX0BpGg79ctVQQAzAV~xdPHx0c3FF3IAZKhp4o5MyRWgDVkOneO2Esa-gRLnCguQfoetbdZ7qtP2lQxofc9v5818LSksB1rqx52xt30nPp1RHA37LP6MYqjNRnTDQWgehGYUMvpXaX-tWcTlwjwB66YDStkVgj6nUkVp2ScccHIC-BzE5kHMQ5GI1jZWVTDDvzyyU-ylprN7FERSqXkcdSL5t-XrSAMU1SuW83uYnZvhCuLoNc~EYcO1GSnfrca2zgePkWyFjoRXx8qOVJ6g3yHecQkzie4AB0DzkD-F0uW9akXgOYDBnA0SBtNWvQ__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
ABL1 promotes apoptosis in BCR-ABL1 leukemia cells in response to genotoxic agents. (A) Results represent mean percentage of clonogenic activity ± SD of BCR-ABL1 Abl1−/− (●) and BCR-ABL1 Abl1+/+ (○) leukemia cells after treatment with indicated DNA damage-inducing agents in the presence (top row) or absence (bottom row) of SCF + IL-3; *P < .05. (B) Western blot analysis of p73, p53, phospho-serine 15 of p53 (phospho-p53) and activated caspase 3 in BCR-ABL1 Abl1−/− [−/−], BCR-ABL1 Abl1+/+ [+/+], and BCR-ABL1/YFP-ABL1 Abl1−/− [−/−(+)] leukemia cells treated with cisplatin (0.25 μg/mL); tubulin served as loading control. (C) Statistically significant (FDR < 0.05) fold changes (>2.0) of expression of indicated genes in BCR-ABL1 Abl1−/− vs BCR-ABL1 Abl1+/+ leukemia cells maintained with SCF + IL-3.
