Back to your search result

Description

A cell-permeable triazine derivative that is shown to increase cellular phosphorylation level of mTOR Ser2448 (20% and 42% above basal in 1 h, respectively, with 1 and 2 µ,M MHY1485) and downstream substrate 4E-BP Thr37/46 (29% and 34% above basal in 1 h, respectively, with 1 and 2 µ,M MHY1485) in rat liver Ac2F cells, affecting culture viability only at much higher concentrations (by 20% after 24 h 20 µ,M treatment). MHY1485 induced cellular LC3-II accumulation in Ac2F (117%, 150%, and 250% of vehicle control LC3-II/LC3-I ratio, respectively, with 0.5, 1, and 2 µ,M treatment for 6 h, 142% and 172% of control ratio, respectively, with 2 µ,M treatment for 1 h or 12 h) is reported to be a result of autophagy inhibition due to reduced fusion between autophagosomes and lysosomes as demonstrated by a reduction of starvation-induced AdGFP-LC3 and lysosome dye co-localization (27% and 32.7% above control co-localization in 6 h serum deprived cultures with or without 2 µ,M MHY1485, 21% above control co-localization with 2 µ,M MHY1485 treatment alone and without serum starvation). The mechanism of mTOR activation by MHY1485 is currently unknown., A cell-permeable triazine derivative that is shown to increase cellular mTOR Ser2448 and downstream substrate 4E-BP Thr37/46 phosphorylation level in rat liver Ac2F cells (1 to 2 µ,M for 1 h), affecting culture viability only at much higher concentrations (by 20% after 24 h 20 µ,M treatment). MHY1485 induced cellular LC3-II accumulation in Ac2F is reported to be a result of autophagy inhibition due to reduced fusion between autophagosomes and lysosomes. The mechanism of mTOR activation by MHY1485 is currently unknown.