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. 2016 Jul 26;6:30529. doi: 10.1038/srep30529

Figure 7. IRF3/HSP90 rather than NF-κB participates in viperin regulation.

Figure 7

(A) In vitro infection with RABV affecting IRF3 expression. RAW264.7 cells were infected with rRC-HL at an MOI of 0.1, and DMSO (for dissolving geldanamycin [GA], an inhibitor of IRF3) was added as a mock control. The cell lysates were prepared and subjected to Western blotting analysis to detect IRF3, Hsp90, viperin, RABV N, and β-actin protein expression. (B) GA inhibits IRF3 and viperin expression. RAW264.7 cells were infected with rRC-HL at an MOI of 0.1 and were treated with 1.0 μM GA. The cell lysates were prepared and subjected to Western blotting analysis to detect IRF3, Hsp90, viperin, RABV N, and β-actin protein expression. (C) The IRF3 and viperin protein/actin ratios in Fig. 3A,B were measured using Li-Cor Odyssey 3.0 analytical software version 29. (D) Mock-treated RAW264.7 cells were infected with rRC-HL at an MOI of 0.1. The cell cultures were used to prepare lysates and were subjected to Western blotting analysis to detect NF-κB (p65), viperin, RABV N, and β-actin protein expression. (E) RAW264.7 cells were infected with rRC-HL at an MOI of 0.1 and then treated with the NF-κB (p65)-specific inhibitor BAY11-7082 to a final concentration of 2.0 μM. The cell cultures were used to prepare lysates and were subjected to Western blotting analysis to detect NF-κB (p65), viperin, RABV N, and β-actin protein expression. (F) The NF-κB and viperin protein/actin ratios in Fig. 3D, E were measured using Li-Cor Odyssey 3.0 analytical software version 29.