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. 2015 May 29;7(6):584–600. doi: 10.1159/000382032

Fig. 2.

Fig. 2

MCMV-mediated mouse Clr-b downregulation is prevented by UV-inactivation and inhibition of early viral and host protein synthesis. a Characterization of mClr-b, MHC-I and Rae-1 expression upon treatment with UV-inactivated MCMV-GFP. Infected NIH3T3 cells were analyzed for surface expression of mClr-b (4A6 mAb), MHC-I (H-2LqDq) and Rae-1 (α-ε). b Quantitation of mClr-b, MHC-I and Rae-1 MFI levels in a relative to mock-treated controls. c Characterization of mClr-b, MHC-I and Rae-1 expression upon MCMV-GFP infections in the presence of various chemical inhibitors. NIH3T3 cells were pretreated with DMSO (controls), ActD (10 nM), CHX (10 μg/ml), PAA (400 μg/ml) or AraC (50 μg/ml), and then infected with MCMV-GFP and analyzed by flow cytometry at 24 h.p.i. d Quantitation of mClr-b, MHC-I and Rae-1 MFI levels in c normalized to DMSO-treated mock MFI levels. Graphs show mean ± SEM. Experiments were analyzed using ANOVA with Bonferroni's post hoc analysis. * p < 0.05, ** p < 0.01, *** p < 0.001. All data are representative of at least 3 independent experiments.