Phospho-FOXO1A (Ser329) Antibody - #AF3416

Fig. 9. EPA targets PGAM2 and activates the PI3K/AKT pathway. A. Heatmap of differentially expressed genes as determined via RNA-seq. B. KEGG pathway analysis of differentially expressed genes. C. The MuSC protein levels of the components of the PI3K/AKT pathway after EPA treatment and PGAM2 interference were measured by western blotting (n = 3). D. ELISA for the effect of EPA after PGAM2 knockdown (n = 3). E. Effect of EPA on the protein levels of components in the PI3K/AKT pathway after knockdown as analyzed by western blotting (n = 2). F–G. Effects of EPA and a PI3K/AKT pathway inhibitor (GDC-0941) on the protein levels of components of the PI3K/AKT pathway in MuSCs (F) and C2C12 cells (G) as determined by western blotting (n = 3). H. Immunofluorescence staining of MyHC to evaluate the differentiation of MuSCs and C2C12 cells. Results are mean ± SEM. ANOVA post-hoc analysis was performed using Fisher's least significant difference test.

Fig. 5.| Effect of E2 treatment (10 nM) on tube formation in trophoblast cells with transfection with human SGK1 shRNA or scrambled shRNA. Tube formation assays were conducted by HUVECs which were cultured in supernatant with or without E2 from the upper transwell chambers containing HTR8/SVneo cells with SGK1 shRNA or scrambled shRNA transfection. Results are shown as mean ± SD (n = 3; * p < 0.05); values without a common symbol represent a significant difference between groups. (B) The levels of p-FOXO1 and FOXO1 in HTR8/SVneo cells were determined by western blotting. GAPDH served as an internal control. Bars are indicated as mean ± SD.(n = 3; #,*p < 0.05); values without a common symbol represent a significant difference between groups

Fig. 4 CTSS deficiency ameliorated stress-related anabolic and catabolic molecular alterations. a–e: Representative immunoblotting images and quantitative data for CTSS, IGF-1, IRS-2, p-PI3K, p-Akt, p-mTOR, p-FoxO1α, MuRF-1, MAFbx1, PGC-1α, PPAR-γ, C-caspase-3, and Bcl-2 in GAS muscles at Day 14 after stress (n = 3). Data are mean ± SEM, and p-values were determined by a one-way ANOVA followed by Bonferroni post hoc tests (b–e). CW: CTSS+/+ control mice, CK: CTSS−/− control mice, SW: 14-day-stressed CTSS+/+ mice, SK: 14-day-stressed CTSS−/− mice. *p 

Fig. 6. |Expression of AKT/FOXO1 signaling pathway (A); mitochondrial function markers(B); BDNF signaling-related proteins (C); and representative confocal microscopy images of BDNF staining (green, magnification: ×40,scale Bar 50 μm) (D: a, 8 M–SED; b, 26 M–SED;c, 18 M–MICT; d, 8 M–MICT); and serum BDNF levels (E); and correlation analysis (F).

Fig. 3. |Nr2e1 deficiency impaired glucose tolerance and insulin sensitivity, the damages were exacerbated by HFD.Western blots measured the expression of phosphorylated protein of IRS1, AKT, GSK3β and FOXO1 in the liver samples after 12 weeks of HFD or SD feeding (3 H). Phosphorylated protein levels were normalized to the respective total protein levels (3I).

Figure 3. |Quxie capsule (QX) regulates the expression of Foxo1 and its regulatory proteins in mouse tumor and spleen tissues. (A) Western blots of Foxo1 and p-Foxo1 protein expression in mouse CT26 colon tumor tissues.