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. 2023 Nov 9;24(22):16110. doi: 10.3390/ijms242216110

Figure 1.

Figure 1

The overexpression of RNF138 inhibited the virus-triggered activations of IRF3 and IFNB1 gene transcription. (A) RNF138 inhibited the IFN-β promoter, ISRE, and NF-κB. HEK293T cells were transfected with the IFN-β, ISRE, and NF-κB reporter and the control or RNF138 plasmid for 24 h and then infected with SeV for 12 h before luciferase assays. (B) The effects of RNF138 on the SeV-induced transcription of downstream genes. HEK293T cells were transfected with the control or RNF138 plasmid for 24 h and then infected with SeV for 8 h before qPCR analysis. (C) Effects of RNF138 on SeV-induced phosphorylation of IRF3 (Ser396, Ser386). HEK293T cells were transfected with the control or myc-RNF138 plasmid for 24 h, then infected with SeV for 8 h before immunoblotting analysis with the indicated antibodies. (D) The effects of RNF138 on the SeV-induced nuclear translocation of IRF3. HEK293T cells were transfected with GFP or RNF138-GFP plasmid for 24 h, then infected with SeV for 8 h. Immunoblot analysis of IRF3 in cytoplasmic (Cyto) and nucleus fractions with the indicated antibodies. ** p < 0.01, *** p < 0.001 (unpaired t-test). Data represent at least two experiments with similar results (mean ± SD, n = 3 independent samples in (A,B,D)).