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. 2016 May 26;11(5):e0156496. doi: 10.1371/journal.pone.0156496

Fig 6. USP18 silencing increases the antiviral activity of IFN-α associated with the JAK-STAT signaling pathway.

Fig 6

(A) Hepg2.2.15 cells were treated with shRR or shUSP18 for 48 hours and then subjected to immunofluorescence analysis using a STAT1-specific polyclonal antibody. Blue, DAPI; green, GFP; red, anti-STAT1; original magnification × 400. Hepg2.2.15 cells were treated with indicated concentration of IFN-α (0, 1, 10, 100, 1000 IU/ml) for 20 hours after either shUSP18 or shRR lentivirus transduction. (B) The protein levels of p-STAT1 and STAT1 were quantified by western blot. (C) STAT1 activation was initiated and prolonged in USP18-silenced HepG2.2.15 cells and STAT1 phosphorylation remained 24 hours after treatment compared to the control group.