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. 2022 Aug 5;37(5):676–684. doi: 10.1016/j.virs.2022.07.013

Fig. 5.

Fig. 5

IFN-β1b-mediated OAS3 induction depends on STAT1 phosphorylation. A The negative control pLKO.1 and STAT1 knockdown (KD) HEK293T cells were treated with 125 U/mL (+) and 250 U/mL (++) IFN-β1b for 24 ​h as indicated, and the expression of endogenous OAS3, STAT1, and p-STAT1 were examined by Western blotting. B The negative control pLKO.1 and STAT3 KD HEK293T cells were treated with 125 U/mL (+) and 250 U/mL (++) IFN-β1b for 24 ​h as indicated, and the expression of endogenous OAS3, STAT1, and p-STAT1 were examined by Western blotting. C The negative control pLKO.1 and STAT1 KD HEK293T cells were infected with EV71 at an MOI of 4, and the expression of endogenous OAS3, STAT1, and p-STAT1 were examined by Western blotting at different time points. D The negative control pLKO.1 and STAT3 KD HEK293T cells were infected with EV71 at an MOI of 4, and the expression of endogenous OAS3, STAT1, and p-STAT1 were examined by Western blotting at different time points. E The negative control pLKO.1, STAT1 KD, and STAT3 KD HEK293T cells were infected with EV71 at an MOI of 4, and the expression levels of OAS3 were examined by RT-qPCR at different time points. The RNA level of “0 ​h” was set as “1”. The results represent the means ​± ​standard deviation from three independent experiments. Statistical significance was analyzed using Student's t-test (# no significance, ∗P ​< ​0.05, ∗∗P ​< ​0.01).