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. 2020 Nov 26;11:6000. doi: 10.1038/s41467-020-19849-9

Fig. 2. β-arrestin 2 positively regulates IFN-β signaling.

Fig. 2

a–d Ifnb, Isg15, and Ccl5 mRNA levels in L929 cells transfected with control or β-arrestin 2 vectors and stimulated with HSV-1 a (**P = 0.0018, ***P < 0.0001, < 0.0001 in sequence, left panel; **P = 0.0040, 0.0028, 0.0050 in sequence, middle panel; ***P = 0.0006, **P = 0.0044, 0.0010 in sequence, right panel), VSV b (***P < 0.0001, **P = 0.0015, 0.0071 in sequence, left panel; ***P < 0.0001, < 0.0001, = 0.0001 in sequence, middle panel; ***P < 0.0001, < 0.0001, = 0.0009 in sequence, right panel), ISD c (***P < 0.0001, left panel; ***P = 0.0004, middle panel; **P = 0.0025, right panel), or poly(I:C) d (***P < 0.0001, left panel; ***P < 0.0001, middle panel; **P = 0.0067, right panel) for indicated times. e, f The virus titers as in a or b for 72 h (**P = 0.0013 in e, **P = 0.0062 in f). g, h Immunoblot of lysates of L929 cells transfected with control or β-arrestin 2 vectors and infected with HSV-1 g or VSV h for indicated times. i, j Immunoblot analysis of monomeric and dimeric STING i and IRF3 j as in g or h. k, l Immunoblot analysis of nuclear and cytoplasmic fractions as in i or j. Data are representative of at least three independent experiments (mean ± SEM in a–f, n = 3). Two-tailed unpaired Student’s t-test.