| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 200mg | 电议 |
MHY1485 is a potent activator of mTOR, which inhibits autophagy and the fusion between autophagosomes and lysosomes.
Cell lines | Ac2F cell |
Preparation Method | Ac2F cells were treated with different concentrations of MHY1485 and 5 µM rapamycin as a positive control for 6 hours. |
Reaction Conditions | 0-2uM MHY1485 for 6 hours |
Applications | MHY1485 has an inhibitory effect on the autophagic process by inhibition of fusion between autophagosomes and lysosomes leading to the accumulation of LC3II protein and enlarged autophagosomes. MHY1485 also induces mTOR activity, providing a possibility for another regulatory mechanism of autophagy by the MHY compound. |
Animal models | 3-4 week old female ICR mice |
Preparation Method | To induce MGC autophagy, mice were injected i.p. with FSH on four successive occasions at 12 h intervals.For activator and inhibitor experiments, MHY1485 (10 mg/kg, 2 days) and chloroquine obtained from Sigma were injected before FSH administration. |
Dosage form | 10 mg/kg MHY1485 for 2 days(intraperitoneal injection) |
Applications | MHY1485 (an agonist of mTOR) significantly suppressed autophagy signaling by activating mTOR. The expression of hypoxia-inducible factor 1-alpha (HIF-1α) was increased after FSH treatment. Blocking hypoxia-inducible factor 1-alpha attenuated autophagy signaling. |
| 产品描述 | MHY1485 is a potent activator of mTOR, which inhibits autophagy and the fusion between autophagosomes and lysosomes[1]. MHY1485 has an inhibitory effect on the autophagic process by inhibition of fusion between autophagosomes and lysosomes leading to the accumulation of LC3II protein and enlarged autophagosomes. MHY1485 also induces mTOR activity, providing a possibility for another regulatory mechanism of autophagy by the MHY compound[2]. In the activation of mTOR in HCC cells MHY1485, gdc inhibited the autophagy activity induced by gdc by upregulating the expression of p-mTOR and downregulating the expression of LC3 and p62[3]. MHY1485 inhibits UV-induced skin cell damages via activating mTOR-Nrf2 signaling[6].MHY1485 treatment inhibited growth and colony formation in both cell lines under irradiation and no-irradiation conditions, results that were not fully consistent with MHY1485's known role in activating mTOR signaling. Combined treatment with MHY1485 and radiation significantly increased apoptosis and senescence in tumor cells in association with oxidative stress, ER stress and p21 stabilization, compared to radiation treatment alone[5]. MHY1485 (an agonist of mTOR) significantly suppressed autophagy signaling by activating mTOR. The expression of hypoxia-inducible factor 1-alpha (HIF-1α) was increased after FSH treatment. Blocking hypoxia-inducible factor 1-alpha attenuated autophagy signaling.[4]. SN potentiated the motor ability in PD mice, promoted the survival of dopaminergic neurons, increased the protein expression level of Beclin1, LC3-II/LC3-I ratio and LC3B-positive neurons, lowered the protein expression level of p62 and inactivated PI3K/AKT/mTOR pathway in the substantia nigra tissue of mouse brains. Moreover, MHY1485 reversed the above effects of SN on PD mice via reactivating PI3K/AKT/mTOR pathway[7]. References: |
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