E1286
Eeyarestatin I
synthetic (organic), ≥98% (HPLC), ERAD inhibitor, powder
别名:
3-（4-氯苯基）-4-[[[（4-氯苯基）氨基] 羰基] 羟基氨基]-5,5-二甲基-2-氧代-1-咪唑烷乙酸 2-[3-（5-硝基-2-呋喃基）-2-丙烯-1-亚基] 酰肼
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关于此项目
经验公式（希尔记法）:
C27H25Cl2N7O7
化学文摘社编号:
分子量:
630.44
MDL number:
UNSPSC Code:
12352204
NACRES:
NA.77
产品名称
Eeyarestatin I, ≥98% (HPLC)
SMILES string
Clc1ccc(cc1)N2C(C(N(C2=O)CC(=O)NN=CC=Cc4[o]c(cc4)[N+](=O)[O-])(C)C)N(O)C(=O)Nc3ccc(cc3)Cl
InChI
1S/C27H25Cl2N7O7/c1-27(2)24(35(40)25(38)31-19-9-5-17(28)6-10-19)34(20-11-7-18(29)8-12-20)26(39)33(27)16-22(37)32-30-15-3-4-21-13-14-23(43-21)36(41)42/h3-15,24,40H,16H2,1-2H3,(H,31,38)(H,32,37)
InChI key
JTUXTPWYZXWOIB-UHFFFAOYSA-N
biological source
synthetic (organic)
assay
≥98% (HPLC)
form
powder
storage condition
desiccated
solubility
DMSO: 5 mg/mL
storage temp.
2-8°C
Quality Level
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Biochem/physiol Actions
Eeyarestatin I 或 Eer1 通过诱导 NOXA 转录因子 ATF3 和 ATF4 的激活，并通过阻断其泛素化来抑制组蛋白 H2A 的降解，从而促进促凋亡蛋白 NOXA 的转录激活。
Eeyarestatin I 是内质网相关蛋白降解 (ERAD) 的强效抑制剂。特异性靶向 p97 相关去泛素化过程 (PAD) 并抑制 ataxin-3 (atx3) 依赖性去泛素化。
Eeyarestatin I 是内质网相关蛋白降解 (ERAD) 的强效抑制剂。特异性靶向 p97 相关去泛素化过程 (PAD) 并抑制 ataxin-3 (atx3) 依赖性去泛素化。也抑制 Sec61 介导的内质网蛋白转位。优先显示对癌细胞的细胞毒活性；通过促凋亡蛋白 NOXA 诱导细胞死亡。
Other Notes
本品为 E/Z 亚胺异构体的混合物
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Qiuyan Wang et al.
Proceedings of the National Academy of Sciences of the United States of America, 106(7), 2200-2205 (2009-01-24)
The ubiquitin-proteasome system has recently emerged as a major target for drug development in cancer therapy. The proteasome inhibitor bortezomib has clinical activity in multiple myeloma and mantle cell lymphoma. Here we report that Eeyarestatin I (EerI), a chemical inhibitor
Jose Lora et al.
The Journal of biological chemistry, 296, 100733-100733 (2021-05-07)
A disintegrin and metalloprotease 17 (ADAM17) is a cell-surface metalloprotease that serves as the principle sheddase for tumor necrosis factor α (TNFα), interleukin-6 receptor (IL-6R), and several ligands of the epidermal growth factor receptor (EGFR), regulating these crucial signaling pathways.
Avantika Gupta et al.
eLife, 9 (2020-06-12)
The transcription factor FoxO has been shown to block proliferation and progression in mTORC1-driven tumorigenesis but the picture of the relevant FoxO target genes remains incomplete. Here, we employed RNA-seq profiling on single clones isolated using laser capture microdissection from
Tatyana Dubnikov et al.
Journal of cell science, 129(19), 3635-3647 (2016-08-24)
Limited detoxification capacity often directs aggregation-prone, potentially hazardous, misfolded proteins to be deposited in designated cytosolic compartments known as 'aggresomes'. The roles of aggresomes as cellular quality control centers, and the cellular origin of the deposits contained within these structures
Garrett E Berry et al.
The Journal of biological chemistry, 291(2), 939-947 (2015-11-04)
Intracellular trafficking of viruses can be influenced by a variety of inter-connected cellular sorting and degradation pathways involving endo-lysosomal vesicles, the ubiquitin-proteasome system, and autophagy-based or endoplasmic reticulum-associated machinery. In the case of recombinant adeno-associated viruses (AAV), proteasome inhibitors are
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