Fig 1: Validation of the expression of the mTOR pathway markers in diabetic nephropathy. (A,B) Box plots of the expression of mTOR pathway markers EIF4B, RICTOR, and PRKCB in control and diabetic nephropathy samples in the (A) GSE111154 and (B) GSE142025 datasets. DN: diabetic nephropathy. (C) H&E staining of the morphology of kidney tissues in the control group and the diabetic nephropathy rat model group. Scale bar, 100 μm; magnification, ×400. (D) The mRNA expression of EIF4B, RICTOR, and PRKCB was determined in kidney tissues from the control and diabetic nephropathy groups through RT-qPCR. (E,F) The expression of EIF4B, RICTOR, and PRKCB proteins was determined in kidney tissues from the control and diabetic nephropathy groups through Western blot. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.
Fig 2: ER expression is elevated in female patients and high-grade/recurrent meningiomas, and correlates with key mTOR pathway components. a) Relative expression score of estrogen receptor (ER) in meningiomas stratified by patient sex (male vs. female). Data are presented as box plots showing median, interquartile range, and outliers. Statistical significance was assessed using the Mann-Whitney U test. P < 0.01. b) Relative ER expression score in meningiomas grouped by WHO grade (WHO I vs. WHO II–III). Significance was determined by Mann-Whitney U test. P < 0.0001. c) ESR2 mRNA expression levels in meningioma samples from the GEO dataset, categorized by WHO grade. Box plots represent median and interquartile ranges; P-values were calculated using Kruskal-Wallis test with Dunn’s post hoc correction. P = 0.0023 for overall comparison. d) ESR mRNA expression in recurrent versus non-recurrent meningiomas from the same GEO dataset. Wilcoxon signed-rank test was used; P < 0.05. e) Representative immunohistochemical staining of ERβin meningioma tissues from female (top row) and male (bottom row) patients. Brown staining indicates positive ERβ expression. Scale bars: 100 μm. f) Western blot analysis of ERβ and mTOR-related proteins (RICTOR, PIK3CA, PTEN, DEPTOR) and loading control (GAPDH) in meningioma tissue lysates from male and female patients. Molecular weight markers are indicated on the right.
Fig 3: 3D hydrogels induce an alternative pathway for hMSCs quiescence. (A–E) Protein expression through western blot analysis to hMSCs cultured in Alginate‐RGD low, Alginate‐RGD high, Collagen, 2D TCPS Control, and Serum‐deprived. Blot figure and relative expression of each condition to 2D TCPS Control of (A) mTOR, (B) Rictor and Raptor (without quantification), (C) AKT (phospho T308), (D) Foxo3 and (E) p27 and RB1 (without quantification). All values are presented as mean ± SD (n = 3), one‐way ANOVA with Dunnett post hoc test, ***p < 0.001. (F) p27 and RB1 immunofluorescence staining on hMSCs encapsulated for 7 days in Alginate‐RGD low, Alginate‐RGD high, and Collagen hydrogels. Nuclei stained in blue (Hoechst). p27 in red and RB1 in green (n = 3); scale bar = 100 µm.
Supplier Page from Abcam for Anti-RICTOR antibody [EPR22008]