Figure 6.
Figure 6. Caspase-3 regulates colony formation of AE-expressing LSCs via autophagy modulation. (A) Average numbers of colonies in the fifth replating resulting from plating 1000 AE9a-expressing fetal liver cells with treatment of MHY1485, an mTOR activator. (B) Average numbers of LTC-IC–driven CFUs in LTC-IC assays resulting from 1000 AE9a-expressing fetal liver cells with treatment of MHY1485, an mTOR activator. (C) The knockdown efficiency of ULK1 in AE-expressing human CD34+ cells. (D) Average number of colonies resulting from 2500 AE-expressing human CD34+ cells with Caspase-3 knockdown by shRNAs (scrambled shRNA served as control) (top panel) and the morphology of the colonies (bottom panel). (E) Working model of the effect of depletion of Caspase-3 on AE(9a)-driven leukemogenesis. DMSO, dimethyl sulfoxide.

Caspase-3 regulates colony formation of AE-expressing LSCs via autophagy modulation. (A) Average numbers of colonies in the fifth replating resulting from plating 1000 AE9a-expressing fetal liver cells with treatment of MHY1485, an mTOR activator. (B) Average numbers of LTC-IC–driven CFUs in LTC-IC assays resulting from 1000 AE9a-expressing fetal liver cells with treatment of MHY1485, an mTOR activator. (C) The knockdown efficiency of ULK1 in AE-expressing human CD34+ cells. (D) Average number of colonies resulting from 2500 AE-expressing human CD34+ cells with Caspase-3 knockdown by shRNAs (scrambled shRNA served as control) (top panel) and the morphology of the colonies (bottom panel). (E) Working model of the effect of depletion of Caspase-3 on AE(9a)-driven leukemogenesis. DMSO, dimethyl sulfoxide.

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