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. 2015 Jul 20;125(8):3103–3116. doi: 10.1172/JCI80924

Figure 2. Defective differentiation of promyelocytes derived from SCN iPSCs is associated with apoptosis, which can be reversed by forced activation of Akt/Bcl2.

Figure 2

(A) FACS dot plot showing annexin V binding on myeloid precursors derived from control (control 12 and control 13), ELANE-mutant SCN iPSCs (SCN15 and SCN14). (B) Quantitation of the % annexin V binding. (C) Relative expression of BCL2 in promyelocytes derived from control and SCN iPSCs. (D) Ectopic expression of murine Bcl2 through retroviral transduction of myeloid precursors derived from SCN iPSCs (SCN15). (E) Ectopic expression of ca-Akt through retroviral transduction of myeloid precursors derived from SCN iPSCs (SCN15). (F) Quantitation of annexin V binding in control-, ca-Akt–, or Bcl2-expressing granulocytic precursors derived from SCN iPSCs. For B and F, data are presented as mean ± SD of 3 independent experiments. For C–E, data are presented as mean ± SD of 2 or more independent experiments in duplicate. Cont, control.