Skip to main content
. 2011 Jun 24;118(7):1865–1876. doi: 10.1182/blood-2010-12-326199

Figure 1.

Figure 1

HBZ activated TGF-β signaling. In 12-well plates, HepG2 cells were cotransfected with 2 ng of phRL-TK, 0.5 μg of reporter plasmid TARE-Luc (A), 3TP-Lux (B), or 9 × CAGA-Luc (C), and 0.5 μg of pcDNA3.1-mycHis-sHBZ. At 24 hours after transfection, the cells were treated with TGF-β (10 ng/mL). After 24 hours, the cells were harvested and analyzed for luciferase activity. Expression of sHBZ was detected by Western blot (middle panel). Coomassie brilliant blue (CBB) staining was shown as the loading control (botom panel). (D) CTLL-2 cells were transfected with 3TP-Lux (2 μg), phRL-TK (10 ng), and pME18Sneo-sHBZ (0.4 μg) by electroporation. Luciferase activity was measured 24 hours after stimulation by TGF-β. (E) In 12-well plates, HepG2 cells were cotransfected with 3TP-Lux (0.5 μg), phRL-TK (2 ng), and pcDNA3.1-mycHis-sHBZ (0, 5, 10, 20, 50, 100, 200, 1000, and 4000 ng). At 24 hours after transfection, the cells were treated with or without TGF-β. After 24 hours, the cells were harvested and analyzed for luciferase activity. mycHis-sHBZ was detected by Western blot (middle panel). CBB staining was shown as the loading control (bottom panel).