Fig 1: Western blotting of SVZ tissues post-TBI. (A) MiR-124-3p affected the expression of neurotrophin signaling pathway molecules after TBI. Western blot (WB) analysis of Akt3, PIK3CA, Ras, phospho-Akt, phospho-PI3K, phospho-MEK1/2, and phospho-Erk1/2 expression in SVZ tissues of TBI rats injected with agomir-124-3p or antagomir-124-3p 5 and 7 days after injury. (B) Statistical analysis of the relative protein expression of each molecule. All proteins analyzed were found to be significantly differentially expressed between the agomir group and antagomir group. (C) The expression of NT-3, BDNF, and DCX in the SVZ tissue was tested 1, 3, 5, and 7 days after TBI. (D) Statistical analysis of the relative protein expression of each molecule. All data are presented as the means ± SD. ? p < 0.05. n = 3/group. Full length western blot scans for the cropped images are presented in Figure S1
Fig 2: PHLDB2 induces EMT by promoting phosphorylation of AKT3. (A) Xiantao website was used to analyze the effect of AKT3 expression on the prognosis of patients with GC. (B) Xiantao was used to analyze the correlation between the expression of AKT3 and EMT markers in GC. (C) The data of TCGA GC were divided into two groups: low-expression group and high-expression group of AKT3. The whole genome expression of these two groups was enriched by GSEA and the enrichment in the EMT pathway was detected by Xiantao. (D) Xiantao was used to analyze the correlation between AKT3 and NR2F1-AS1/miR-190a/PHLDB2 expression in GC. (E,F) The expression of PHLDB2, PI3K, AKT3, and p-AKT was detected by WB after transfection of PHLDB2-OE(EV) and NR2F1-AS1-OE(EV) into BGC823 and SGC7901 cell lines. (G) PHLDB2-OE and EV were transfected into BGC823 and SGC7901 with stable knockout-AKT3 or knockout-control to detect the expression of p-AKT and EMT markers by WB. *p < 0.05; **p < 0.01; ***p < 0.001.
Supplier Page from Abcam for Anti-AKT3 (phospho S472) + AKT2 (phospho S474) + AKT1 (phospho S473) antibody [EPR18853]