Fig. 2. Effects of G3BP1 knockdown on virus-triggered signaling.

a Effects of G3BP1-RNAi plasmids on exogenous or endogenous G3BP1 expression. b–d G3BP1 knockdown inhibits SeV-induced IFN-β promoter, ISRE, and Nifty. Stable G3BP1-RNAi knockdown cells (1 × 10⁵) were transfected with the IFN-β reporter, ISRE and Nifty (0.1 μg), and TK (0.02 μg) for 24 h, and then uninfected or infected with SeV for 12 h before luciferase assays. The experiment was repeated in triplicates. e–g G3BP1 knockdown inhibits poly (I:C)-induced IFN-β promoter, ISRE, and Nifty. Stable G3BP1-knockdown HEK293T cells (1 × 10⁵) were transfected with the IFN-β reporter, ISRE, Nifty (0.1 μg), and TK (0.02 μg) for 24 h, and then transfected with poly (I:C) (1 μg/ml) for 18 h before luciferase assays were performed. The experiment was repeated in triplicates. h Effects of G3BP1 knockdown on SeV-induced phosphorylation of TBK1, IRF3, P65, and Iκbα. Stable G3BP1-knockdown HEK293T cells were infected or uninfected with SeV for the indicated time before immunoblotting was performed. For the phosphorylation of TBK1, IRF3, P65, and Iκbα, band intensities were determined by Image J software. Data are mean ± SD of three independent experiments. *P < 0.05, **P < 0.01, two-tailed t-test. Coni control-RNAi, Luc luciferase.