Extended Data Fig. 1: The expression of Shisa9 is up-regulated during HSV-1 infection.
From: Modulation of virus-induced neuroinflammation by the autophagy receptor SHISA9 in mice
(a) Wild-type (WT) mice (n = 3 mice per group) were intravenously infected (HSV-1) or uninfected (UI) with HSV-1 (1 × 105 PFU) for 5 days, then real-time quantitative polymerase chain reaction (qPCR) analysis was performed of indicated Shisa genes in the brain. Results were normalized to gapdh and presented as log2 (values). (b) qPCR analysis of SHISA9 in indicated human brain cell lines with or without HSV-1 (MOI = 1) infection for 24 hrs. qPCR analysis of Shisa9 in mice microglia cell line BV2 with HSV-1(MOI = 1) infection for indicated time periods. (c) U87 cells were transfected with control siRNA or SHISA2-9 siRNA for 24 hrs, and then infected with HSV-1 (MOI = 1) for 24 hrs. Cell lysates were collected to determine SHISA2-9 knockdown efficiency by qPCR. Cell supernatants were collected to detect IL-6 production by ELISA. (d) Schematic presentation of generation of Shisa9−/− mice through CRISPR/Cas9 technology. (e) Sequencing analysis of Shisa9−/− mice. In (b-c), all error bars, mean values ± SEM, P-values were determined by unpaired two-tailed Student’s t test of 3 independent biological experiments.
