Fig. 2
From: MLL5 suppresses antiviral innate immune response by facilitating STUB1-mediated RIG-I degradation
MLL5 suppresses RLR-mediated immune signaling. a Immunoblot analysis of phosphorylated (p-) IRF3 and P65 in WT and Mll5−/− MEFs upon infection with VSV-GFP (MOI:1). Actin served as a loading control. b Immunoblot analysis of IRF3 and P65 protein in nuclear and cytoplasmic fractions in WT and Mll5−/− MEFs infected with VSV-GFP (MOI:1). Actin served as a cytoplasmic control. Lamin B1 served as a nuclear protein control. c WT and MLL5−/− HEK293T cells were transiently transfected with indicated reporter plasmids (200 ng) along with MLL5-expressing plasmids (0, 100, 300, and 600 ng). After 24 h, a luciferase assay was performed with stimulation of intracellular poly(I:C) (1 μg/ml) for 16 h. Results were presented relative to the luciferase activity in control cells (transfected with luciferase reporter and empty vector without stimulation of intracellular poly(I:C)). Immunoblot analysis of MLL5-FLAG are shown below. Actin served as a loading control. Data were representative of three independent experiments with similar results (a, b) or were from three independent experiments (c), and were analyzed by Student’s t-test (two-tailed) and were presented as mean ± SD (*p < 0.05,**p < 0.01,***p < 0.001, ****p < 0.0001)
