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. 2008 Jul 17;27(15):2147–2157. doi: 10.1038/emboj.2008.143

Figure 3.

Figure 3

K7 inhibits IRF activation at the level of TBK1/IKKɛ. In (A–G), HEK293 cells were transfected with pRK5-K7R or pRK5-A52R, together with the indicated luciferase reporter genes for 24 h. Data are expressed as the mean fold induction±s.d. relative to control levels, for a representative experiment of at least two, each performed in triplicate. (A, B) Cells were transfected with IRF7-GAL4 (A) or IRF3-GAL4 (B) expression plasmids, and the GAL4-dependent pFR luciferase reporter gene plus 50 ng expression plasmid encoding TRIF. (C) Cells were transfected with the Ifnb promoter reporter gene prior to sendai virus infection for 16 h. (D) Cells were transfected with the ISRE reporter gene plus 50 ng MAVS expression plasmid. (E, F) Cells were transfected with IRF7-GAL4 and the pFR luciferase reporter gene, plus 50 ng of either TBK1 (E) or IKKɛ (F) expression plasmid. (G) Cells were transfected with the ISRE reporter gene plus 50 ng of either TBK1 or IRF7 expression construct for 24 h. (H) Schematic of SeV signalling pathway to Ifnb promoter induction. The deduced point of inhibition by K7 is marked with an asterisk. (I) For the IRF transactivation assay, cells were transfected as in (B), followed by stimulation with SeV for 16 h (upper panel). For immunoblot analysis, cells were transfected with K7, followed by SeV stimulation for 6 h. Western blots were probed for total IRF3 and phosphorylated IRF3 (Ser396) (lower panel).