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Image Search Results
Journal: Autophagy
Article Title: Modulating FKBP5/FKBP51 and autophagy lowers HTT (huntingtin) levels.
doi: 10.1080/15548627.2021.1904489
Figure Lengend Snippet: Figure 10. Comparing SAFit2 and rapamycin in HD NSC. (A) Left panel. CASP3-CASP7 activity normalized to protein levels in C116 and HD NSC treated for 24 h in starvation medium with 0.1% DMSO vehicle, 1 µM SAFit2 (two-way ANOVA, *p ≤ 0.05), or 1 µM rapamycin (two-way ANOVA, **p ≤ 0.01). right panel. CASP3-CASP7 activity normalized to protein levels in HD NSC treated for 24 h in starvation media with 0.1% DMSO vehicle, 1, 1.5 and 2 µM SAFit2 (two-way ANOVA, **p ≤ 0.001), or 1, 1.5, and 2.0 µM rapamycin (two-way ANOVA, ***p ≤ 0.001). The two first bars on the left are full media (NPM), media with 0.1% DMSO vehicle, and starvation medium with 0.1% DMSO vehicle. (B,C,D) Quantification of the expression levels of p-RPS6 (B), p-MTOR (C), and p-ULK (D) in C116 and HD NSC after 48 h of treatment with either 0.1% DMSO vehicle, 10 µM SAFit2, or 10 µM rapamycin treatment. analysis of quantified levels indicates significant reduction in phosphorylated RPS6 with 10 µM rapamycin (one-way ANOVA, ****p ≤ 0.0001, and one-way ANOVA, ***p ≤ 0.001) in C116 and HD NSC, respectively, when compared to vehicle control. SAFit2 treatment did not significantly alter levels of phosphorylated RPS6 when compared to control. Analysis of quantified levels indicates significant reduction in phosphorylated MTOR with 10 µM rapamycin (one-way ANOVA, ***p ≤ 0.001, and one-way ANOVA, ****p ≤ 0.0001) in C116 and HD NSC, respectively, when compared to vehicle control.Again, SAFit2 treatment did not significantly alter levels of phosphorylated MTOR when compared to control. analysis of quantified levels indicates significant reduction in phosphorylated ULK1 with 10 µM rapamycin in C116 NSC (one-way ANOVA, *p ≤ 0.05). In HD NSC, treatment with 10 µM SAFit2 significantly increased phosphorylated ULK1 (one-way ANOVA, *p ≤ 0.05) when compared to control.
Article Snippet: Primary antibody phosphorylated MTOR (1:100; Cell Signaling Technology, 2971), was normalized to total
Techniques: Activity Assay, Expressing, Control
Journal: BMC cancer
Article Title: Astaxanthin-loaded PLGA nanoparticles inhibit survival of MKN-45 gastric cancer cell line by modulating JAK2/STAT3/mTOR/PI3K pathway.
doi: 10.1186/s12885-024-13401-4
Figure Lengend Snippet: Fig. 9 Values obtained from Western blotting and FOLD of Control tests for the expression of GAPDH, JAK2, P-JAK2, STAT3, P-STAT3, mTOR,P-mTOR, and PI3K proteins in all four groups of control, ASX, PLGA and ASX+PLGA
Article Snippet: Primary antibodies GAPDH((6C5) Santa Cruz-32233), JAK2((C-10): Santa Cruz-390539), P-JAK2((Tyr 1007/Tyr 1008)-R: Santa Cruz-16566-R), STAT3(AB_2565913 (BioLegend Cat. No. 678002)), P-STAT3(AB_10897947 (BioLegend Cat. No. 651001)),
Techniques: Western Blot, Control, Expressing
Journal: PLoS ONE
Article Title: Synergistic Effects of Targeted PI3K Signaling Inhibition and Chemotherapy in Liposarcoma
doi: 10.1371/journal.pone.0093996
Figure Lengend Snippet: SW872 and SW982 cells were treated with different concentrations of PI-103 for 24 hours. The effects of PI-103 on PI3K/mTOR pathway protein expression levels were determined by West blot analysis. Note the significant decrease in pAKT and p4EBP1 expression in both of liposarcoma cell lines post PI-103 treatment.
Article Snippet: The human AKT, phosphorylated AKT (pAKT) (threonine [Thr]308), PI3K p110α, phosphorylated 4E binding protein 1 (p4EBP1) (Thr37/46), BcL-XL, Cytochrome c, caspase 3, mTOR,
Techniques: Expressing