Fig 1: Immunohistochemistry for AKT1, GTSE1, BIRC5, AURKA, PBK, KNSTRN, and PSMB10. Samples from cancer-adjacent endometrial tissue (N = 75) and endometrial cancer (N = 107). Cancer-adjacent endometrial tissue sample of weak immunostaining score for either AKT1 (A), GTSE1 (D), BIRC5 (G), AURKA (J), PBK (M), KNSTRN (P), and PSMB10 (S). Endometrial cancer sample of weak and strong immunostaining score for either AKT1 (B,C), GTSE1 (E,F), BIRC5 (H,I), AURKA (K,L), PBK (N,O), KNSTRN (Q,R), and PSMB10 (T,U). The expression for each gene were depicted in (V) slides (200 X, *p < 0.05, **p < 0.01).
Fig 2: Graphic representation of macrophage LMP10 in diet-induced atherosclerosis. The accumulation of lipids (such as ox-LDL) induces macrophage LMP10 expression, which facilitates the degradation of phosphorylated I?Ba, followed by activation and translocation of phosphorylated NF-?B p65, finally promoting macrophage polarization and inflammation, therefore contributing to atherosclerosis.
Fig 3: LMP10 deletion inhibited diet-induced aortic macrophage infiltration and polarization in ApoE ko mice. (A,B) Flow cytometry analysis of aortic total macrophage infiltration (A) and M1/M2-type macrophage numbers (B) after 8 weeks of ATD. n = 4–5 per group. (C) Real-time PCR analysis of aortic M1- and M2-associated inflammatory cytokine expression after 8 weeks of ATD. n = 6 per group, *p < 0.05; **p < 0.01; ns, not significant.
Fig 4: Stub1 deletion enhances antigen processing and presentation by sensitizing tumour cells to IFN?. (a–c) Flow cytometry analysis of cell surface MHC-I on parental, control or independent Stub1-null B16-F10 cells. gMFI, geometric mean fluorescence intensity. (d, e) Western blot analysis of the expression level of STUB1, STAT1, STAT2, IRF1, PSMB8, PSMB9 and PSMB10 in parental, control or independent Stub1-null B16-F10 cells. Band intensity was normalized with total protein signal. The tumour cells were either untreated (Nil) or treated with IFN? for 24 h (a–e). See Supplementary Fig. 1 for additional flow cytometry plots, Western blot data and analysis (a, d, e). (f) Western blot analysis of the expression level of IRF1, STAT1, and phosphorylation of Tyr701-STAT1 at 2 h post-treatment with IFN? (twofold serial dilution from 2.0 ng ml-1). (g) Volcano plot showing differential presentation of MHC-associated peptide in gStub1 #1 versus gControl cells, following stimulation with 0.03 ng ml-1 IFN? for 24 h. Red circles highlight peptides significantly enriched in gStub1 #1 cells (twofold cutoff, P = 0.01; n = 3 biological replicates). FC, fold change. See Supplementary Fig. 2d for data of gStub1 #2 cells. Representative of four (a) or two (d–f) independent experiments. Data are mean ± s.d. (b) or mean with all data points (c) from four independent experiments. P values were determined by ordinary two-way ANOVA on Log2-transformed data with Dunnett’s multiple comparisons test, ****P = 0.0001 (c).
Fig 5: LMP10 was abundantly expressed in lesional macrophages in diet-induced atherosclerosis in ApoE ko mice. (A) Western-blot analysis and quantitation of aortic LMP10 protein expression in ApoE ko mice before and after 8 weeks of ATD feeding. n = 4 per group, **p < 0.01. (B) Immunofluorescent co-staining of LMP10 with CD68 or SM22a in the aortic root of ApoE ko mice before and after 8 weeks of ATD feeding.
Supplier Page from Abcam for Anti-PSMB10/MECL1 antibody [EPR14902]