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A, B
Virus‐induced phosphorylation of TBK1 and IRF3 in cytoplasmic (CE) and nuclear (NE) extracts of WT and XAF1‐deficient BMDMs was measured by IB.
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C
Monomeric and dimeric IRF3 expression (top blot) in whole‐cell lysates of WT and XAF1‐deficient BMDMs stimulated with VSV‐WT (MOI = 1) was measured by IB.
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D
ChIP assays were performed, and the results were quantified by qRT–PCR to detect IRF3 binding to an ISRE in WT and XAF1‐deficient BMDMs activated by VSV‐WT (MOI = 1) for 9 h.
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E
IB was performed to determine the VSV‐induced phosphorylation level of STAT1.
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F
HEK293T cells were transfected with IFN‐β luciferase reporters in the presence (+) or absence (−) of the indicated XAF1 expression plasmids. Luciferase assays were used to determine the fold change in expression with respect to the empty vector group 36 h after transfection.
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G
qRT–PCR analysis of Irf7 mRNA in WT and XAF1‐deficient BMDMs stimulated with distinct virus infections.
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H, I
IB analysis of VSV‐ or HSV‐1‐induced IRF7 expression as measured in whole‐cell lysates of WT and XAF1‐deficient BMDMs.
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J
ChIP assays were performed and quantified by qRT–PCR to detect IRF7 binding to an ISRE in WT and XAF1‐deficient BMDMs stimulated with VSV‐WT (MOI = 1) or HSV‐1.
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K–N
WT and XAF1MKO mice crossed with mice with an IRF7−/− background were i.n. infected with a sublethal dose (0.1 hyaluronic acid [HA]) of the H1N1 strain PR8. The survival rate (K, n = 15), viral titer in the lung (L, n = 5), serum IFN‐β level (M, n = 5), and intensity of H&E‐stained lung tissue sections (N, n = 5) were determined at the indicated time points. Scale bar, 200 μm.