Figure 1
From: TRIM26 facilitates PRV infection through NDP52-mediated autophagic degradation of MAVS
TRIM26 promotes replication of PRV. A Western blot analysis of TRIM26 protein levels in PK-15 cells after 0, 12, 24 and 36 h of infection with PRV at an MOI of 0.01. GAPDH was used as the protein loading control. B mRNA levels of EP0 in PK-15 cells after 0, 12, 24 and 36 h of infection with PRV at an MOI of 0.01. C PK-15 cells transfected with TRIM26-HA (0.25 μg, 0.5 μg, or 1 μg) were infected with PRV (MOI = 0.001) at 16 h, and the level of PRV replication was detected by Western blotting at 24 h. GAPDH was used as the protein loading control. D and E The mRNA levels of EP0 were detected by qPCR (D), and the virus supernatant was collected for the TCID50 assay (E). F and G Construction of a TRIM26-deficient cell line using CRISPR/Cas9. TRIM26 deficiency was verified by Western blotting (F) and gel electrophoresis (G); sequences within TRIM26 were targeted by sgRNA 1 and sgRNA 2 (blue). TGG and GGG (red) are the protospacer adjacent motif (PAM), and “ × ” indicates the knockout sites. H TCID50 analysis of PRV after 12 and 24 h of infection at an MOI of 0.01. The data are shown as the mean ± SD of three independent experiments; * p < 0.1; ** p < 0.01; *** p < 0.001.