American Society of Hematology

Figure 4

$Figure 4. Induction of ER stress in HL60 cells activates PDI and thereby suppresses CEBPA protein. (A-E) Real-time PCR assessing mRNAs for PDI (A), GRP78 (B), CHOP (C), CEBPA (D), and calreticulin (CRT; E) from HL60 cells treated for 24 hours with 3 μg/mL tunicamycin, 3.7 μg/mL calcimycin, or DMSO as control. Error bars indicate SD based on 3 independent experiments. (F) Western blot of the cytoplasmic fraction (CF) and whole-cell lysates (WCL) from HL60 cells treated with 3 μg/mL tunicamycin for 24 hours. Membranes were stained with Abs against PDI, GRP78, calreticulin (CRT), and CEBPA. β-actin was used as loading control.$

Induction of ER stress in HL60 cells activates PDI and thereby suppresses CEBPA protein. (A-E) Real-time PCR assessing mRNAs for PDI (A), GRP78 (B), CHOP (C), CEBPA (D), and calreticulin (CRT; E) from HL60 cells treated for 24 hours with 3 μg/mL tunicamycin, 3.7 μg/mL calcimycin, or DMSO as control. Error bars indicate SD based on 3 independent experiments. (F) Western blot of the cytoplasmic fraction (CF) and whole-cell lysates (WCL) from HL60 cells treated with 3 μg/mL tunicamycin for 24 hours. Membranes were stained with Abs against PDI, GRP78, calreticulin (CRT), and CEBPA. β-actin was used as loading control.

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