EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #73262_C
泛素-蛋白酶体抑制剂；NF-κB通路抑制剂；IκB激活剂
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总览
(S)-MG132是一种可逆的、细胞渗透性蛋白酶体活性抑制剂(IC₅₀ = 100 nM；Kisselev & Goldberg)和钙蛋白酶（Calpain）的抑制剂 (IC₅₀= 1.2µM；Tsubuki等人)。泛素-蛋白酶体通路选择性地降解细胞内蛋白，从而清除受损或错误折叠的蛋白，并调节参与控制炎症过程和细胞周期调节的关键蛋白的可用性(S)-MG132 通过抑制 IκB 的降解来抑制NF-κB 的激活（IC₅₀ = 3 µM；Arlt 等人，Palombella 等人，Ortiz-Lazareno 等人）。
癌症研究
·阻断HeLa细胞DNA损伤引发的细胞凋亡（Zhang等人）。
·抑制NF-κB激活，使多种癌细胞对凋亡敏感（Arlt等人）。
·对多种人类癌细胞系的细胞毒性作用（Banerjee & Liefshitz）。
·抑制小鼠黑色素瘤（B16）和人眼部黑色素瘤（IPC227F）细胞系的生长（Vivier等人）。
细胞类型
癌细胞及细胞系
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
研究领域
癌症
CAS 编号
133407-82-6
化学式
C₂₆H₄₁N₃O₅
纯度
≥98%
通路
NF-κB，泛素
靶点
IκB，蛋白酶体
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
相关材料与文献
技术资料 (2)
文献 (8)
MG132 inhibition of proteasome blocks apoptosis induced by severe DNA damage. Cell cycle (Georgetown, Tex.) 2011
Abstract
The 26S proteasome, a multicatalytic enzyme complex, is the main intracellular proteolytic system involved in the degradation of ubiquitinated proteins. The ability of proteasome inhibitors to induce apoptosis has been exploited in the recent development of chemotherapeutic agents. Here, we show that inhibition of proteasome by MG132 blocks DNA damage-induced apoptosis. Blockage of apoptosis by MG132 correlates with p53 stabilization and upregulation of p21/WAF1, a p53 transcriptional target. Surprisingly, in the absence of MG132, robust apoptosis induced by a high dose of UV irradiation correlate with rapid p53 degradation. This is in sharp contrast to p53 stabilization when cells were exposed to lower levels of UV irradiation. Our findings highlight a scenario in which severe UV damage can induce rapid p53 degradation by the proteasome. Importantly, these data suggest that the 26S proteasome plays a key role in promoting apoptosis induced by high doses of UV irradiation.
Synthesis, radiosynthesis, and biological evaluation of new proteasome inhibitors in a tumor targeting approach. Journal of medicinal chemistry 2008
Abstract
Proteasome inhibition is a new strategy in cancer therapy. We synthesized three new peptide aldehyde inhibitors linked to the benzamide derivative structure to use their cytotoxic activity against malignant melanoma cells. Of these, 10 displayed the highest cytotoxicity (0.18 +/- 0.16 microM). A radiosynthesis of the iodine aldehyde was performed. Its drug biodistribution showed that some selectivity of the benzamide group toward malignant melanoma tissue was conserved.
MG132 proteasome inhibitor modulates proinflammatory cytokines production and expression of their receptors in U937 cells: involvement of nuclear factor-kappaB and activator protein-1. Immunology 2008
Abstract
In response to inflammatory stimuli, monocytes/macrophages secrete greater quantities of the proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and IL-6. The inflammatory process and the innate immune response are related to the activation of several transcription factors, such as nuclear factor kappaB (NF-kappaB) and activator protein 1 (AP-1). The proteasome is a multimeric protease complex, which plays a vital role in several cellular functions, including the regulation of transcription factors like NF-kappaB. In this study, we used the human monocyte cell line U937 stimulated with lipopolysaccharide (LPS) and phorbol 12-myristate 13-acetate (PMA) as a model to investigate the in vitro effects of MG132, a proteasome inhibitor, on the release of TNF-alpha, IL-1beta and IL-6 and on the expression of their membrane and soluble receptors TNF-R1, IL-1R1 and IL-6R. We also analysed the effects of MG132 on the activation of NF-kappaB and AP-1 and on the IkappaB molecule. MG132 significantly inhibited the secretion of those proinflammatory cytokines. MG132 increased the release of the soluble receptors TNF-R1 and IL-1R1 from U937 cells and decreased their cell-surface expression. MG132 also increased IL-6R cell-surface expression and decreased its release. Proteasome inhibition also led to an increase in LPS+PMA-induced AP-1 activation and the attenuation of LPS+PMA-induced IkappaB degradation, resulting in the abolition of NF-kappaB activation. Our experiments strongly suggest that the proteasome is an important factor in the regulation of proinflammatory cytokines and their receptors.
更多信息
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
|---|---|
| Cas Number | 133407-82-6 |
| Chemical Formula | C₂₆H₄₁N₃O₅ |
| 纯度 | ≥ 98% |
| Target | IκB, Proteasome |
| Pathway | NF-κB, Ubiquitin |
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