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. 2020 Jan 8;10:2962. doi: 10.3389/fmicb.2019.02962

FIGURE 1.

FIGURE 1

Classical swine fever virus (CSFV) inhibits NDP52 (CALCOCO2) ubiquitination and SUMOylation. (A) PK-15 cells were infected with CSFV (MOI = 0.1) or un-infected (MOCK) at the indicated time points. CALCOCO2, Npro, and GAPDH levels were analyzed by Western blot. (B) After CSFV infection, CALCOCO2 mRNA was detected by qRT-PCR. The data represent the mean ± SD of three independent experiments. Data were tested by one-way ANOVA with Fisher’s least significant difference (LSD) post hoc correction. P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; #P > 0.05. (C) PK-15 cells were infected with CSFV. NDP52 SUMOylation was analyzed by immunoblot using anti-SUMO2-4 antibody. SUMO2-4 expression in CSFV-infected cells was used as the input control. (D) Ubiquitinated NDP52 was immunoblotted with anti-Ub(A-5) antibody. Ub(A-5) expression in CSFV-infected cells was used as the input control. GAPDH was used as the internal loading control.