Skip to main content
. 2020 Oct 30;10(26):12223–12240. doi: 10.7150/thno.50992

Figure 3.

Figure 3

TAB1-mediated p38α activation facilitates for HCV replication. (A-C) Inhibitory effect of p38α knockdown on HCV replication in Huh7.5.1 cells. Huh7.5.1 cells were transfected with control siRNA (NC) or siRNA specific for p38 (p38-RNAi #1 and #2) and infected with the HCV JFH1 strain. The expression levels of p38, P-p38, and the HCV core protein were determined by western blotting (A), and the intracellular (B) and extracellular (C) HCV RNA levels were determined by qRT-PCR. (D-F) Promotion effect of p38α overexpression on HCV replication in Huh7.5.1 cells. Experiments were performed as described above, except the cells were transfected with the control or p38α expression plasmid. (G-I) Effect of p38α on the rescue of HCV replication in p38α-knockdown Huh7.5.1 cells. P38α was knocked down (KD) using CRISPR/Cas9 and p38α was reintroduced into p38α-knockdown cells (KD+p38α). The HCV core protein, p38 and GAPDH were measured by western blotting (G). The intracellular (H) and extracellular (I) HCV RNA levels were measured by qRT-PCR. (J) Abolishing effect of p38α activation site mutation on the promotion of p38α to HCV replication. Flag-p38α and Flag-p38αAF plasmids were expressed in p38α-knockdown Huh7.5.1 cells, and HCV infection was detected. (K) Impaired effect of TAB1 knockdown on HCV replication in Huh7.5.1 cells. WT and KD-TAB1 cells were infected with JFH1, and the HCV core protein was detected by western blotting.