产品名称
MHY1485, ≥95% (HPLC)
SMILES string
[N+](=O)([O-])c1ccc(cc1)Nc2nc(nc(n2)N4CCOCC4)N3CCOCC3
InChI
1S/C17H21N7O4/c25-24(26)14-3-1-13(2-4-14)18-15-19-16(22-5-9-27-10-6-22)21-17(20-15)23-7-11-28-12-8-23/h1-4H,5-12H2,(H,18,19,20,21)
InChI key
MSSXBKQZZINCRI-UHFFFAOYSA-N
assay
≥95% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear (warmed)
storage temp.
2-8°C
Quality Level
相关类别
Application
MHY1485已被用于：
- 研究哺乳动物雷帕霉素靶蛋白mTOR信号传导对 体外 O-GlcNAcylation糖基化修饰的作用
- 抑制自我吞噬
- 作为mTOR 激动剂证明 O-连接N-乙酰葡糖胺转移酶- RNA解旋酶 p68 (OGT-DDX5) 调节结肠直肠癌细胞的增殖和转移。
Biochem/physiol Actions
MHY1485是mTOR激活剂，可通过抑制自噬体和溶酶体之间的融合，有效抑制自噬。
MHY1485是mTOR激活剂：自噬抑制剂。
MHY1485结合雷帕霉素（mTOR）的哺乳动物靶标，并刺激其作用。MHY1485可以穿透细胞。它防止紫外诱导的角化细胞和成纤维细胞的氧化应激。
Features and Benefits
这种化合物是细胞凋亡研究的特色产品。点击此处发现更多特色细胞凋亡产品。在sigma.com/discover-bsm可了解更多关于生物活性小分子的其他研究领域。
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Rui Ma et al.
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas, 54(12), e11183-e11183 (2021-10-21)
Due to the high mortality and rapid disease progression, ovarian cancer remains one of the most common malignancies threatening the health of women. The present study was conducted to explore the anticancer effects and the underlying mechanisms of poricoic acid
Cross regulation between mTOR signaling and O-GlcNAcylation
Very N, et al.
Journal of Bioenergetics and Biomembranes, 50(3), 213-222 (2018)
Duc-Vinh Pham et al.
Journal of experimental & clinical cancer research : CR, 41(1), 9-9 (2022-01-07)
Adiponectin, the most abundant adipokine derived from adipose tissue, exhibits a potent suppressive effect on the growth of breast cancer cells; however, the underlying molecular mechanisms for this effect are not completely understood. Fatty acid metabolic reprogramming has recently been
MHY1485 ameliorates UV-induced skin cell damages via activating mTOR-Nrf2 signaling
Yang Bo, et al.
Oncotarget, 8(8), 12775-12775 (2017)
ULK1 phosphorylates Sec23A and mediates autophagy-induced inhibition of ER-to-Golgi traffic
Gan W, et al.
BMC Cell Biology, 18(1), 22-22 (2017)
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