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. 2019 Jun 18;29(8):641–654. doi: 10.1038/s41422-019-0193-0

Fig. 1.

Fig. 1

Identification of virus-induced IFN-I-dependent lncLrrc55-AS in macrophages. a cDNA of lncLrrc55-AS in VSV-infected mouse peritoneal macrophages. b RT-qPCR analysis of lncLrrc55-AS in macrophages infected with SeV for 12 h. c RT-qPCR analysis (left) of the distribution of different RNAs following nucleus/cytoplasm fractionation of macrophages infected with SeV for 12 h. Western blot analysis (right) of nucleus/cytoplasm fractionation. d FISH analysis of lncLrrc55-AS in macrophages infected with SeV for 12 h. Scale bar, 20 µm. e, f RT-qPCR analysis of lncLrrc55-AS expression in macrophages infected with HSV for 12 h, or stimulated with poly(I:C) for 12 h, LPS for 3 h (e), or IFNβ with the indicated dose for 8 h (f). g, h RT-qPCR analysis of lncLrrc55-AS expression in WT and Irf3−/− macrophages infected with SeV or VSV for 12 h (g), in WT and Ifnar1−/− macrophages treated with IFNα4, IFNβ (500 U/mL) for 8 h or infected with SeV for 12 h (h). i RT-qPCR analysis of lncLrrc55-AS expression in macrophages pretreated for 1 h with the JAK inhibitor Baricitinib (2 μM) or the STAT1 inhibitor Fludarabine (1 μM), then infected with SeV or VSV for 12 h or treated with IFNα4 for 8 h. Data are from three independent experiments (b, c left, e–i, means ± SEM) or are representative of three independent experiments with similar results (a, c right, d). ***P < 0.005 (Student’s t-test or ANOVA)