Phospho-RPS6 (Ser235) Antibody - #AF3354

Fig. 5. Disordered iron homeostasis and inhibited mTORC1 activity upon exposure to CdCl2 and PCB77 at low dose. (A) The relative fluorescence intensity of CAeAM for measuring LIP to reflect intracellular iron availability (n = 3–4), and (B) Representative blots of FTH1 protein content to reflect iron storage. Analyses were performed after single or combined exposure to CdCl2 and PCB77 at 1 μM for 48 h. (C) Phosphorylated S6 and total S6 content to re- flect mTORC1 activity as measured by Western blot. Ratio of FTH1 to eIF2αP and ratio of pS6 to S6 in the control group were defined as 1. Analyses were performed after single or combined exposure to CdCl2 and PCB77 at 1 μM for 48 h. a- significantly different from the control group. Data were presented in mean ± SE. P < 0.05 was considered statistically significant.

Fig. 5 Ketogenic diet activated mTORC2 in the heart of spontaneously hypertensive rats. a The phosphorylation of AMPK and the ratio of p-S6/S6 and p-Akt/Akt in the heart of Wistar rats and SHRs were measured with Western blots. The quantitative result were shown in b–d. Values are the mean ± SEM. n = 4 for each group. *P < 0.05, **P < 0.01

Fig. 5 H2O2 induces GC autophagy through the mTOR and Ras-cAMPPKA signaling pathway. Primary cultured GC were treated with H2O2 (200 μmol/l) for different time periods. Then, the GC samples were analyzed by immunoblotting using the corresponding antibody. a The expression of mTOR protein was determined by western blotting. b The expression of PI3K, AKT, and RPS6 was determined by western blotting c The expression of Ras, cAMP, and PKA was determined by western blotting. d–j The relative expression of p-mTOR, p-PI3K, p-AKT, pRPS6, Ras, cAMP, and PKA were quantified by software Image J. Data represent as the means ± SE from three independent experiments. * p < 0.05, ** p < 0.01