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SML1135

Sigma-Aldrich

MG-132(R)

≥95% (HPLC)

同義詞:

ZL-LEU-d-LEU-L-LEU-al

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About This Item

經驗公式(希爾表示法):
C26H41N3O5
CAS號碼:
分子量::
475.62
MDL號碼:
分類程式碼代碼:
12352200
PubChem物質ID:
NACRES:
NA.32

產品線

SAFC Hitech®

品質等級

化驗

≥95% (HPLC)

形狀

powder

溶解度

DMSO: soluble

儲存溫度

−20°C

SMILES 字串

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 密鑰

TZYWCYJVHRLUCT-ZRBLBEILSA-N

基因資訊

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。

法律資訊

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

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable


分析證明 (COA)

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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)
Yinfeng Xu et al.
FEBS letters, 593(15), 1974-1982 (2019-06-04)
The tumor protein p53-inducible nuclear protein 2 (TP53INP2) has been reported to participate in autophagy by interacting with autophagosome-localized autophagy-related protein 8 (Atg8) family proteins, including LC3. Here, we uncover a novel function for TP53INP2 in the autophagic degradation of
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
Yalong Wang et al.
Neuroscience letters, 739, 135402-135402 (2020-09-26)
Synaptotagmin-11 (Syt11) is associated with schizophrenia and Parkinson's disease (PD) and is a critical substrate of parkin, an E3 ubiquitin ligase linked to PD. Previously we reported that Syt11 regulates multiple membrane trafficking pathways in neurons and glia. However, the
Corinna Wentzel et al.
Nature communications, 9(1), 267-267 (2018-01-20)
Here we explore the relationship between presynaptic homeostatic plasticity and proteasome function at the Drosophila neuromuscular junction. First, we demonstrate that the induction of homeostatic plasticity is blocked after presynaptic proteasome perturbation. Proteasome inhibition potentiates release under baseline conditions but

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