IFN-α upregulates C/EBPβ expression irrespective of the presence of BCR-ABL signaling. (A) Schematic illustration of the experimental protocol. EML cells were treated with 100 U/mL IFN-α for 0.5 or 3 hours, with or without 12-hour treatment with 1 μM imatinib (IM). (B) Western blotting analysis of EML cells transduced with empty or BCR-ABL expression vector. Representative data from 3 independent experiments are shown. Cebpb is a single-exon gene; the 3 isoforms, liver activating protein (LAP)*, LAP, and liver inhibitory protein (LIP), are translated from different start codons. These blots are representative of at least 3 independent experiments. (C) Blot intensity was quantified using ImageJ and normalized against the corresponding level of GAPDH. The level of the LAP isoform in nontreated, empty vector-transduced EML cells was defined as 1.0, and the average relative expression levels of LAP under each condition from 4 different blots were plotted. Data are means ± standard deviation (SD) of 3 independent experiments. Results were normalized against the corresponding level of GAPDH protein. (D) IFN-α–induced Cebpb mRNA expression in EML cells transduced with empty or BCR-ABL expression vectors. Data are means ± SD of 3 independent experiments. Results were normalized against the corresponding level of Gapdh mRNA. *P < .05; **P < .01.