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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
human ... CTSB(1508) , NFKB1(4790) , PSMA1(5682)
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
The effect of MG132, a proteasome inhibitor on HeLa cells in relation to cell growth, reactive oxygen species and GSH.
Oncology Reports, 22(1), 215-221 (2009)
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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
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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
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
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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