Fig. 6

IFN-γ inhibits the activation of notch signaling. a Flow cytometry plots showing the expression of notch1 on the LSK cells and DN cells of mice, GKO mice, and IFN-γ overexpressing mouse livers (a) and the expression of notch2 on LSK cells and DN cells of C57BL/6j mice, GKO mice, and IFN-γ overexpressing mouse BM (c) (n = 5–10). b, d Statistical analysis of the expression of notch1 (b) and notch2 (d) on LSK cells and DN cells of mice, GKO mice, and IFN-γ overexpressing mouse livers and BM. Bars represent the mean ± SEM of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001. e The gene expression level of ligands of notch signal on the LSEC in the WT and GKO mice. Bars represent the mean ± SEM of three independent experiments. *P < 0.05. f The gene expression level of Notch downstream targets Hes1 and Hes5 on the LSK cells in the liver and BM of IFN-γ overexpressing mice, WT, and GKO mice. g The LSK cells of the liver and BM were sorted from WT mice and incubated in the indicated conditions of ruxolitinib (10 μM) for 1 h before stimulation with 100 ng/ml IFN-γ for 30 min. Levels of β-actin as well as total and phospho-Tyr701 STAT1 were determined using immunoblotting. h As in (g), the gene expression level of Hes1 and Hes5 on the LSK cells of the liver and BM in ruxolitinib-treated mice and the control mice were detected. Bars represent the mean ± SEM of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001