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

Fig. 7. Carvedilol promoted cGAS–STING activation through β-arrestin 2.

Fig. 7

a, b Ifnb, ISG15, and Ccl5 mRNA in WT peritoneal macrophages infected for 16 h with HSV-1 a (***P < 0.0001 in all panels) or VSV b (***P = 0.0002, ***P < 0.0001, ***P < 0.0001) and then treated with PBS or carvedilol. c, d The virus titers as in a or b for 72 h (**P = 0.0058 in c, **P = 0.0050 in d). e, f Immunoblot of lysates of peritoneal macrophages from WT mice infected with HSV-1 e or VSV f for indicated times and treated with PBS or carvedilol. g, h Immunoblot analysis of monomeric and dimeric IRF3 as in e or f. i, j Immunoblot analysis of nuclear and cytoplasmic fractions as in e or f. k Immunoassay of lysates of HEK293T cells transfected with various vectors and treated with PBS or carvedilol. l Immunoassay of cell lysates and streptavidin-precipitated proteins from HEK293T cells transfected with various vectors and stimulated with biotin-ISD and carvedilol. m cGAMP activity measured by extracts from HT-DNA-stimulated (6 h) WT peritoneal macrophages treated with PBS or carvedilol. n Immunoblot analysis of monomeric and dimeric STING as in g. o, p Immunoassay of lysates of peritoneal macrophages infected with HSV-1 o or VSV p for indicated times and treated with PBS or carvedilol. Data are representative of at least three independent experiments (mean ± SEM in a–d, n = 3). **P < 0.01 and ***P < 0.001, two-tailed unpaired Student’s t-test.