产品名称
ISRIB, ≥98% (HPLC)
质量水平
方案
≥98% (HPLC)
表单
powder
颜色
white to beige
溶解性
DMSO: 1 mg/mL, clear (warmed)
储存温度
2-8°C
SMILES字符串
ClC1=CC=C(OCC(N[C@@H]2CC[C@@H](NC(COC3=CC=C(Cl)C=C3)=O)CC2)=O)C=C1
InChI
1S/C22H24Cl2N2O4/c23-15-1-9-19(10-2-15)29-13-21(27)25-17-5-7-18(8-6-17)26-22(28)14-30-20-11-3-16(24)4-12-20/h1-4,9-12,17-18H,5-8,13-14H2,(H,25,27)(H,26,28)/t17-,18-
InChI key
HJGMCDHQPXTGAV-IYARVYRRSA-N
应用
ISRIB(综合应激反应抑制剂)已被用作综合应激反应的抑制剂。
生化/生理作用
ISRIB 是一种血脑屏障渗透剂,是内质网应激适应性受损的有效选择性综合应激反应 (ISR) 抑制剂。ISRIB 是 PERK 信号的有效抑制剂,可有效逆转 eIF2a 磷酸化作用,恢复细胞翻译能力。ISRIB 增强啮齿类动物的认知记忆。
ISRIB 是一种血脑屏障渗透剂,是强效选择性 PERK 信号通路抑制剂;认知记忆增强剂。
ISRIB(综合应激反应抑制剂)作为一种药物,赋予细胞抵抗真核起始因子2(eIF2)α磷酸化(如激活转录因子4(ATF4)和真核翻译起始因子4E(eIF4E)结合)的下游作用的抗性 蛋白质1(4E-BP1)诱导。
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Z D Kabir et al.
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Loss of galactose-1 phosphate uridylyltransferase (GALT) activity in humans results in Classic Galactosemia, and the GalT-deficient (GalT-/-) mouse mimics the patient condition. GalT-/- ovaries display elevated endoplasmic reticulum (ER) stress marker, BiP, and downregulated canonical phosphatidylinositol 3-kinase (Pi3k)/protein kinase B
Caitlin M Rodriguez et al.
Nature neuroscience, 23(3), 386-397 (2020-02-19)
Repeat-associated non-AUG-initiated translation of expanded CGG repeats (CGG RAN) from the FMR1 5'-leader produces toxic proteins that contribute to neurodegeneration in fragile X-associated tremor/ataxia syndrome. Here we describe how unexpanded CGG repeats and their translation play conserved roles in regulating
Sara K Young-Baird et al.
Molecular cell, 77(4), 875-886 (2019-12-15)
Dysregulation of cellular protein synthesis is linked to a variety of diseases. Mutations in EIF2S3, encoding the γ subunit of the heterotrimeric eukaryotic translation initiation factor eIF2, cause MEHMO syndrome, an X-linked intellectual disability disorder. Here, using patient-derived induced pluripotent stem
Vivek Kumar Pandey et al.
Cellular signalling, 59, 41-52 (2019-03-17)
Hyperglycemia associated ER stress has been found as a critical contributor in the pathogenesis of type 2 diabetes mellitus. However, reports regarding molecular mechanisms involved are limited. This study was aimed to identify the role of ER stress in regulating
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