图1：CSDE1是VSV复制的正调节器。没有siRNA，阴性对照siRNA或[S15373+15374 siRNA]（2 csde1特异性siRNA）46和CSDE1在24或48小时后通过Western斑点分析的CSDE1水平。（代表三个单独的实验）。B – D在用siRNA转染后48小时与A中的HEP3B细胞被VSV-GFP感染（MOI 0.1）。48小时（b）或96 h（c）后来，通过斑块测定法确定病毒滴度，D在感染后96小时计算存活细胞的数量。两个独立实验的代表。E B16-，B16-CSDE1C-T-或B16-CSDE1WT过表达的细胞在MOI为0.1时被VSV-IFN-β感染。二十四，48和72小时后，通过斑块测定在BHK细胞上测量病毒滴度。三个独立实验的代表。F fenthe Hep3b细胞或均衡的野生型CSDE1WT或突变体CSDE1C-T被VSV-IFN-β（MOI 0.1）感染（3井/组）。 Forty-eight hours later (Passage 1), supernatants were assayed for infectious titers on the same cells on which the virus was passaged. Virus was recovered every 48 h (P2–5) and similarly titered. Representative of three separate experiments. G Stock VSV-IFN-β virus or VSV-IFN-β, which had been passaged five times through Hep3B parental or Hep3B-CSDE1C-T cells as in F, was titered on either Hep3B parental cells or on Hep3B-CSDE1C-T cells. Representative of two separate experiments. Means ± SD of three technical replicates are shown. P-values were determined using a one-way (B–D) or two-way (E–G) ANOVA with a Tukey’s multiple comparisons post test on log-transformed data. Statistical significance was set at p < 0.05, ns > 0.05. Source data are provided as a Source Data file. Credit: DOI: 10.1038/s41467-021-22115-1
