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. 2016 Jun 2;7(6):e2239. doi: 10.1038/cddis.2016.146

Figure 5.

Figure 5

Effects of TMEM2 on the translocation of IRF9 into nuclei and the expression of MxA and OAS1. (a) IRF9 localization was analyzed by IFA. The level of IRF9 in the nuclei of HepG2 shTMEM2 cells did not change significantly in response to HBV infection compared with that in HepG2 GFP cells. In contrast, the level of IRF9 in the nuclei of non-HBV-infected HepG2 TMEM2 cells was remarkably higher than that in non-HBV-infected HepG2 GFP and HepG2 shTMEM2 cells. HBV infection reduced the level of IRF9 in the nuclei in HepG2 TMEM2 cells. Similar results were observed in HepG2.2.15 cells, which overexpressed TMEM2; nuclear translocation is represented by column shown on the right side of Figure 5a. (b) Using a plasmid that expresses a reporter gene (firefly luciferase) under the control of a promoter containing ISRE motifs, we showed that transfection of this plasmid into HepG2 TMEM2 cells, either with HBV infection or without, significantly increased luciferase activity compared with HepG2 GFP and HepG2 shTMEM2 cells (*P<0.05 compared with HepG2 GFP cells without HBV infection; #P<0.05 compared with HepG2 GFP cells with HBV infection). Similar results were observed in TMEM2-overexpressing HepG2.2.15 cells ($P<0.05 compared with HepG2.2.15 GFP cells without HBV infection, ^P<0.05 compared with HepG2.2.15 GFP cells with HBV infection). When TMEM2 was silenced in HepG2 cells, the luciferase activity was markedly reduced. Error bars are presented as S.D.