Figure 6.
Induction of UPR does not cause increased fold change in apoptosis in CLPB variant–expressing myeloid cells. The myeloid cell line MOLM-13 was transduced with CLPB variants or empty vector control, and cells were sorted based on GFP positivity. Cells were treated with DMSO (D) or the glycosylation-inhibitor tunicamycin (TM) for 24 hours. (A) Induction of the UPR was confirmed by assessing expression of HSPA5 by quantitative polymerase chain reaction. The percentage of cleaved caspase-3+ (B) or Annexin V+ (C) cells was assessed by flow cytometry. Fold change representation of cleaved caspase-3+ (D) or Annexin V+ (E) cells expressed as the ratio of TM/DMSO within each sample. Data represent 3 independent experiments. *P < .05, **P < .01, ***P < .001, repeated-measures 1-way ANOVA.

Induction of UPR does not cause increased fold change in apoptosis in CLPB variant–expressing myeloid cells. The myeloid cell line MOLM-13 was transduced with CLPB variants or empty vector control, and cells were sorted based on GFP positivity. Cells were treated with DMSO (D) or the glycosylation-inhibitor tunicamycin (TM) for 24 hours. (A) Induction of the UPR was confirmed by assessing expression of HSPA5 by quantitative polymerase chain reaction. The percentage of cleaved caspase-3+ (B) or Annexin V+ (C) cells was assessed by flow cytometry. Fold change representation of cleaved caspase-3+ (D) or Annexin V+ (E) cells expressed as the ratio of TM/DMSO within each sample. Data represent 3 independent experiments. *P < .05, **P < .01, ***P < .001, repeated-measures 1-way ANOVA.

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