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. 2020 Aug 19;28(2):640–656. doi: 10.1038/s41418-020-00609-7

Fig. 7. RNF220 mediates type 2 IFN and HSV-1 infection.

Fig. 7

a, b Gene expression analysis of Rnf220, Cxcl9, Cxcl10, Mx1, Irf1, and Tnf in WT and Rnf220+/– BMDMs in response to IFN-γ treatment (10 ng/ml, a) and HSV-1 infection (3 MOI, b) for indicated times. c Immunoblot analysis of RNF220 in WT and Rnf220+/– BMDMs in response to IFN-γ treatment (10 ng/ml) and HSV-1 infection (3 MOI) for indicated times. d Immunoblot analysis of phosphorylation of STAT1, STAT3, and ERK in WT and Rnf220+/– BMDMs in response to IFN-γ treatment and HSV-1 infection for indicated times. e Immunoblot analysis of STAT1 dimerization in Stat1–/– L929 cells transfected with WT FLAG-STAT1, mutated FLAG-STAT1 (K110R), WT HA-STAT1, and RNF220 plasmids as indicated with or without IFN-γ treatment. f, g WT and Rnf220+/– mice were intranasally infected with HSV-1 (5.0 × 106 pfu per mouse) for 2 days and pulmonary viral burden was analyzed by qRT-PCR (f) and plaque assay (g). Each symbol indicates an individual mouse for f and g. Data represent two independent experiments and are presented as mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; ns not significant.