S100A9 Antibody - #DF7596

Fig. 5 Characterizing endothelial cell subsets within the tumor microenvironment of breast cancer. A Single-cell map showing endothelial cell subsets. B UMAP plots of 1425 endothelial cells from eight patient samples. C UMAP showing single-cell profiles of endothelial cells in the angiogenic and non-angiogenic groups. D Endothelial cell subcluster composition for different patients. E Scatter plot showing differences in the distribution of endothelial cell subclusters between angiogenic negative and positive groups. The ecology of angiogenic and non-angiogenic breast cancer groups. F–G Violin plot and UMAP figure showing the expression of markers related to angiogenesis and exosomes in these endothelial cell subsets and individual distribution. H Immunofluorescence images of CXCR4, S100A9 and PPP1R1B expression, which are highly specific in the angiogenesis group and distribution of marker genes. Scale bar, 20 µm. I Representative IHC images of gene signatures

Fig. 5 Characterizing endothelial cell subsets within the tumor microenvironment of breast cancer. A Single-cell map showing endothelial cell subsets. B UMAP plots of 1425 endothelial cells from eight patient samples. C UMAP showing single-cell profiles of endothelial cells in the angiogenic and non-angiogenic groups. D Endothelial cell subcluster composition for different patients. E Scatter plot showing differences in the distribution of endothelial cell subclusters between angiogenic negative and positive groups. The ecology of angiogenic and non-angiogenic breast cancer groups. F–G Violin plot and UMAP figure showing the expression of markers related to angiogenesis and exosomes in these endothelial cell subsets and individual distribution. H Immunofluorescence images of CXCR4, S100A9 and PPP1R1B expression, which are highly specific in the angiogenesis group and distribution of marker genes. Scale bar, 20 µm. I Representative IHC images of gene signatures

Figure 5. OSM suppresses HBV replication through the JAK-STAT signaling pathway. (A) Extracts from HepG2.2.15 cells treated with OSM (20 ng/mL) for 0∼60 minutes were analyzed for STAT activation. (B) HepG2.2.15 cells were pretreated with ruxolitinib (1 μM) and the AG490 (10 μM) for 1 hour and then were treated with OSM (20 ng/mL) for 10 minutes. The phosphorylation levels of STAT1, STAT3, and STAT5 were examined by immunoblotting. (C, E) The supernatant HBsAg and HBV DNA levels were examined in the indicated groups. One-way analysis of variance. (D) The inhibition effects of OSM on intracellular HBV RNAs and HBV antigens were analyzed in HepG2.2.15 cells pretreated with or without ruxolitinib. Inhibition ratios of OSM for intracellular pgRNA and total RNA for the indicated cell lines were calculated as (1 - OSM-treatment/sham-treatment) ×100. Relative gray values of HBsAg and HBcAg were analyzed by Image J and normalized to β-actin. Unpaired t test. (F) The expression levels of IRFs in HepG2.2.15 cells treated with OSM were examined by quantitative polymerase chain reaction and immunoblotting. Unpaired t test. (G) STAT1-IRF9 heterodimer formation was examined by coimmunoprecipitation in Huh7-1.3 cells treated with OSM. ∗P < .05, ∗∗P < .01, and ∗∗∗P < .001.