Merck
CN

SML1135

Sigma-Aldrich

MG-132(R)

≥95% (HPLC)

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别名:
ZL-LEU-d-LEU-L-LEU-al
经验公式(希尔记法):
C26H41N3O5
分子量:
475.62
MDL编号:
PubChem化学物质编号:
NACRES:
NA.32

产品线

SAFC Hitech®

质量水平

检测方案

≥95% (HPLC)

形式

powder

溶解性

DMSO: soluble

储存温度

−20°C

SMILES字符串

O=C(N[C@H](CC(C)C)C(N[C@H](C=O)CC(C)C)=O)[C@H](CC(C)C)NC(OCC1=CC=CC=C1)=O

InChI

1S/C26H41N3O5/c1-17(2)12-21(15-30)27-24(31)22(13-18(3)4)28-25(32)23(14-19(5)6)29-26(33)34-16-20-10-8-7-9-11-20/h7-11,15,17-19,21-23H,12-14,16H2,1-6H3,(H,27,31)(H,28,32)(H,29,33)/t21-,22+,23-/m0/s1

InChI key

TZYWCYJVHRLUCT-ZRBLBEILSA-N

基因信息

相关类别

生化/生理作用

MG-132(R)是一种有效的膜透性蛋白酶体抑制剂。以10μM的浓度,它诱导PC12细胞中的神经突向外生长。BXI-132(R)可阻断聚(ADP-核糖)聚合酶的切割和胸腺细胞的凋亡。然而,MG-132(R)还可激活c-Jun N-末端蛋白激酶(JNK-1),其可响应细胞应激而启动细胞凋亡。蛋白酶体抑制可诱导热休克蛋白mRNA的积累、热休克蛋白的激活、以及增强各种细胞类型中的耐热性。

法律信息

SAFC Hitech is a registered trademark of Sigma-Aldrich Co. LLC

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable


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Xueyan Zhao et al.
Developmental and comparative immunology, 106, 103632-103632 (2020-01-29)
Tightly regulation of NF-κB signaling is essential to innate and adaptive immune responses, but its regulatory mechanism remains unclear in various organisms, especially teleost fish. In this study, we reported that IRF3 attenuates the inhibitory effect of IκBα on NF-κB
The effect of MG132, a proteasome inhibitor on HeLa cells in relation to cell growth, reactive oxygen species and GSH.
Han YH
Oncology Reports, 22(1), 215-221 (2009)
Fanjie Jin et al.
Oncology letters, 19(1), 858-868 (2020-01-04)
The clinical significance of the proteasome inhibitor MG132 has been examined in numerous human cancer types; however, its influence on the metastasis and progression of pancreatic cancer is yet to be determined. In the present study, the effect of MG132
Shashipavan Chillappagari et al.
Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society, 20(1), 140-148 (2020-06-15)
The stress-regulated enzyme hemeoxygenase-1 (HO-1) contributes to the cell response towards inflammation and oxidative stress. We previously reported on curtailed HO-1 expression in cystic fibrosis (CF) bronchial epithelial (CFBE41o-) cells and CF-mice, but the molecular mechanisms for this are not
Ling-Yun Chu et al.
Scientific reports, 7(1), 12472-12472 (2017-10-01)
Pro-inflammatory cytokines are known to induce endothelial cell autophagy, but the role of autophagy in regulating the expression of pro-inflammatory molecules has not been characterized. We hypothesized that autophagy facilitates expression of endothelial adhesion molecules. TNFα and IL-1β induced autophagy

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