Figure 5.
Figure 5. The phenotype of AE9a-Caspase-3−/− or AE-Caspase-3−/− cells induced by Caspase-3 deficiency can be rescued by ULK1 inhibition. (A) Average colony numbers in the fifth replating resulting from plating of 1000 AE9a-expressing fetal liver cells with ULK1 knockdown by shRNAs. (B) Average number of LTC-IC–driven CFUs in LTC-IC assays resulting from 1000 AE9a-expressing fetal liver cells with ULK1 knockdown by shRNAs. (C) The knockdown efficiency of ULK1 in AE9a-Caspase-3−/− leukemia cells before transplantation. (D) The survival of recipient mice transplanted with AE9a-Caspase-3−/− leukemia cells expressing shULK1s were shorter than AE9a-Caspase-3−/− leukemia cells expressing scrambled shRNA in a secondary transplantation model. (E-F) Four weeks after transplantation, the recipient mice transplanted with AE9a-Caspase-3−/− leukemia cells expressing shULK1s had higher WBC counts and more GFP+ (AE9a-expressing) cells. PB, peripheral blood.

The phenotype of AE9a-Caspase-3−/− or AE-Caspase-3−/− cells induced by Caspase-3 deficiency can be rescued by ULK1 inhibition. (A) Average colony numbers in the fifth replating resulting from plating of 1000 AE9a-expressing fetal liver cells with ULK1 knockdown by shRNAs. (B) Average number of LTC-IC–driven CFUs in LTC-IC assays resulting from 1000 AE9a-expressing fetal liver cells with ULK1 knockdown by shRNAs. (C) The knockdown efficiency of ULK1 in AE9a-Caspase-3−/− leukemia cells before transplantation. (D) The survival of recipient mice transplanted with AE9a-Caspase-3−/− leukemia cells expressing shULK1s were shorter than AE9a-Caspase-3−/− leukemia cells expressing scrambled shRNA in a secondary transplantation model. (E-F) Four weeks after transplantation, the recipient mice transplanted with AE9a-Caspase-3−/− leukemia cells expressing shULK1s had higher WBC counts and more GFP+ (AE9a-expressing) cells. PB, peripheral blood.

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