![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=1720811666&Signature=s8ZKXxp19G9cnUddrnImJQatGKK4DV9p5uHa-zql0SjvtY7-yZTVHPve-fDM1HgcbJjkwgrDF5Zamwmt9Kp9zZgPoqggFEj6aw8DfSZrw50EZf~byKpmnNop1fv44k52Xhk--kN-ZyZwG9xX0VX2fbprzl0NPMZVVqIjnwARqhioTX4sfACA27BjVTfCS8Vz96HKOpuOYG5EzPVeWGgnX88wjbi9PHkT~EHX7CzrkrylouU-Tgg7cnA9Ebb6L~p1ETgBQ5-821am3mtdAFOqecnEzzLGpgeNuNrxhV4LWGFiBlt4F~ucKAgUC5OqMpD796huOAB7yRPWavCG6BogLQ__&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.
