• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

泛素化和 NF-κB 抑制剂的降解。

Ubiquitination and degradation of the inhibitors of NF-kappaB.

机构信息

Department of Immunology and Genetics and Biotechnology, Hebrew University-Hadassah Medical School, Institute of Medical Research Israel-Canada, Jerusalem, 91120, Israel.

出版信息

Cold Spring Harb Perspect Biol. 2010 Feb;2(2):a000166. doi: 10.1101/cshperspect.a000166.

DOI:10.1101/cshperspect.a000166
PMID:20182612
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2828279/
Abstract

The key step in NF-kappaB activation is the release of the NF-kappaB dimers from their inhibitory proteins, achieved via proteolysis of the IkappaBs. This irreversible signaling step constitutes a commitment to transcriptional activation. The signal is eventually terminated through nuclear expulsion of NF-kappaB, the outcome of a negative feedback loop based on IkappaBalpha transcription, synthesis, and IkappaBalpha-dependent nuclear export of NF-kappaB (Karin and Ben-Neriah 2000). Here, we review the process of signal-induced IkappaB ubiquitination and degradation by comparing the degradation of several IkappaBs and discussing the characteristics of IkappaBs' ubiquitin machinery.

摘要

NF-κB 激活的关键步骤是 NF-κB 二聚体从其抑制蛋白中释放出来,这是通过 IkappaB 的蛋白水解实现的。这种不可逆的信号转导步骤构成了转录激活的承诺。该信号最终通过 NF-κB 的核排出而终止,这是基于 IkappaBalpha 转录、合成和 IkappaBalpha 依赖性 NF-κB 核输出的负反馈环的结果 (Karin 和 Ben-Neriah 2000)。在这里,我们通过比较几种 IkappaB 的降解并讨论 IkappaB 的泛素机制的特点,来回顾信号诱导的 IkappaB 泛素化和降解的过程。

相似文献

1
Ubiquitination and degradation of the inhibitors of NF-kappaB.泛素化和 NF-κB 抑制剂的降解。
Cold Spring Harb Perspect Biol. 2010 Feb;2(2):a000166. doi: 10.1101/cshperspect.a000166.
2
Regulation of NF-κB by ubiquitination and degradation of the IκBs.IκBs 的泛素化和降解对 NF-κB 的调节。
Immunol Rev. 2012 Mar;246(1):77-94. doi: 10.1111/j.1600-065X.2012.01098.x.
3
Hydrogen peroxide prolongs nuclear localization of NF-kappaB in activated cells by suppressing negative regulatory mechanisms.过氧化氢通过抑制负调控机制延长活化细胞中核因子κB的核定位。
J Biol Chem. 2008 Jul 4;283(27):18582-90. doi: 10.1074/jbc.M801312200. Epub 2008 May 12.
4
Nuclear ubiquitin ligases, NF-kappaB degradation, and the control of inflammation.核泛素连接酶、核因子-κB降解与炎症控制
Sci Signal. 2008 Jan 8;1(1):pe1. doi: 10.1126/stke.11pe1.
5
Nuclear IKKbeta is an adaptor protein for IkappaBalpha ubiquitination and degradation in UV-induced NF-kappaB activation.核 IKKβ是一种衔接蛋白,在 UV 诱导的 NF-κB 激活中,它能够促进 IkappaBα的泛素化和降解。
Mol Cell. 2010 Aug 27;39(4):570-82. doi: 10.1016/j.molcel.2010.07.030.
6
Phosphorylation meets ubiquitination: the control of NF-[kappa]B activity.磷酸化与泛素化相遇:NF-κB活性的调控
Annu Rev Immunol. 2000;18:621-63. doi: 10.1146/annurev.immunol.18.1.621.
7
PDLIM2-mediated termination of transcription factor NF-kappaB activation by intranuclear sequestration and degradation of the p65 subunit.PDLIM2通过细胞核内隔离和p65亚基的降解介导转录因子NF-κB激活的终止。
Nat Immunol. 2007 Jun;8(6):584-91. doi: 10.1038/ni1464. Epub 2007 Apr 29.
8
IL-17 receptor signaling: ubiquitin gets in on the act.白细胞介素-17受体信号传导:泛素参与其中。
Sci Signal. 2009 Oct 13;2(92):pe64. doi: 10.1126/scisignal.292pe64.
9
COMMD1 promotes the ubiquitination of NF-kappaB subunits through a cullin-containing ubiquitin ligase.COMMD1通过一种含cullin的泛素连接酶促进NF-κB亚基的泛素化。
EMBO J. 2007 Jan 24;26(2):436-47. doi: 10.1038/sj.emboj.7601489. Epub 2006 Dec 21.
10
Nuclear retention of IkappaBalpha protects it from signal-induced degradation and inhibits nuclear factor kappaB transcriptional activation.IκBα 的核内滞留保护其免受信号诱导的降解,并抑制核因子κB 的转录激活。
J Biol Chem. 1999 Mar 26;274(13):9108-15. doi: 10.1074/jbc.274.13.9108.

引用本文的文献

1
Multiomics profiles of genome-wide alterations in H3K27ac in different lung lobes after acute graft--host disease with MSCs treatment.急性移植物抗宿主病经间充质干细胞治疗后不同肺叶中H3K27ac全基因组改变的多组学图谱。
Front Immunol. 2025 May 15;16:1570916. doi: 10.3389/fimmu.2025.1570916. eCollection 2025.
2
Investigating Natural Product Inhibitors of IKKα: Insights from Integrative In Silico and Experimental Validation.研究IKKα的天然产物抑制剂:基于计算机模拟与实验验证相结合的见解
Molecules. 2025 May 2;30(9):2025. doi: 10.3390/molecules30092025.
3
TLR4 endocytosis and endosomal TLR4 signaling are distinct and independent outcomes of TLR4 activation.Toll样受体4(TLR4)的内吞作用和内体TLR4信号传导是TLR4激活的不同且独立的结果。
EMBO Rep. 2025 Apr 9. doi: 10.1038/s44319-025-00444-2.
4
Ubiquitination of Immune System and Cancer Therapy.免疫系统的泛素化与癌症治疗。
Adv Exp Med Biol. 2024;1466:35-45. doi: 10.1007/978-981-97-7288-9_3.
5
E3 ubiquitin ligase gene modulates TNF-induced cell death pathways and promotes aberrant proliferation in rheumatoid arthritis fibroblast-like synoviocytes.E3 泛素连接酶基因调节 TNF 诱导的细胞死亡途径,并促进类风湿关节炎成纤维样滑膜细胞的异常增殖。
Front Immunol. 2024 Sep 5;15:1433898. doi: 10.3389/fimmu.2024.1433898. eCollection 2024.
6
Potential Application of Plant-Derived Compounds in Multiple Sclerosis Management.植物源化合物在多发性硬化症治疗中的潜在应用。
Nutrients. 2024 Sep 5;16(17):2996. doi: 10.3390/nu16172996.
7
TRAF3 loss-of-function reveals the noncanonical NF-κB pathway as a therapeutic target in diffuse large B cell lymphoma.肿瘤坏死因子受体相关因子3功能缺失揭示非经典核因子κB信号通路可作为弥漫性大B细胞淋巴瘤的治疗靶点。
Proc Natl Acad Sci U S A. 2024 Apr 30;121(18):e2320421121. doi: 10.1073/pnas.2320421121. Epub 2024 Apr 25.
8
Activity-based profiling of cullin-RING E3 networks by conformation-specific probes.基于构象特异性探针的 Cullin-RING E3 网络的活性分析。
Nat Chem Biol. 2023 Dec;19(12):1513-1523. doi: 10.1038/s41589-023-01392-5. Epub 2023 Aug 31.
9
HSPB1 facilitates chemoresistance through inhibiting ferroptotic cancer cell death and regulating NF-κB signaling pathway in breast cancer.热休克蛋白家族成员 B1(HSPB1)通过抑制铁死亡和调控 NF-κB 信号通路促进乳腺癌的化疗耐药。
Cell Death Dis. 2023 Jul 15;14(7):434. doi: 10.1038/s41419-023-05972-0.
10
Degron Pathways and Leishmaniasis: Debating Potential Roles of spp. Proteases Activity on Guiding Hosts Immune Response and Their Relevance to the Development of Vaccines.降解途径与利什曼病:关于 spp. 蛋白酶活性在引导宿主免疫反应中的潜在作用及其与疫苗开发相关性的辩论
Vaccines (Basel). 2023 May 23;11(6):1015. doi: 10.3390/vaccines11061015.

本文引用的文献

1
An inhibitor of NEDD8-activating enzyme as a new approach to treat cancer.一种NEDD8激活酶抑制剂作为治疗癌症的新方法。
Nature. 2009 Apr 9;458(7239):732-6. doi: 10.1038/nature07884.
2
Modification by single ubiquitin moieties rather than polyubiquitination is sufficient for proteasomal processing of the p105 NF-kappaB precursor.单泛素部分修饰而非多聚泛素化就足以实现p105核因子-κB前体的蛋白酶体加工。
Mol Cell. 2009 Feb 27;33(4):496-504. doi: 10.1016/j.molcel.2009.01.023.
3
Proteolysis of NF-kappaB1 p105 is essential for T cell antigen receptor-induced proliferation.NF-κB1 p105的蛋白水解对于T细胞抗原受体诱导的增殖至关重要。
Nat Immunol. 2009 Jan;10(1):38-47. doi: 10.1038/ni.1685. Epub 2008 Dec 7.
4
New insights into NF-kappaB regulation and function.对核因子-κB调控与功能的新见解。
Trends Immunol. 2008 Oct;29(10):469-78. doi: 10.1016/j.it.2008.07.003. Epub 2008 Sep 3.
5
The Cdc14B-Cdh1-Plk1 axis controls the G2 DNA-damage-response checkpoint.Cdc14B-Cdh1-Plk1轴调控G2期DNA损伤反应检查点。
Cell. 2008 Jul 25;134(2):256-67. doi: 10.1016/j.cell.2008.05.043.
6
UV as an amplifier rather than inducer of NF-kappaB activity.紫外线作为核因子-κB活性的增强剂而非诱导剂。
Mol Cell. 2008 Jun 6;30(5):632-41. doi: 10.1016/j.molcel.2008.03.017.
7
Introducing spatial information into predictive NF-kappaB modelling--an agent-based approach.将空间信息引入预测性核因子-κB建模——一种基于智能体的方法。
PLoS One. 2008 Jun 4;3(6):e2367. doi: 10.1371/journal.pone.0002367.
8
Understanding NF-kappaB signaling via mathematical modeling.通过数学建模理解核因子-κB信号通路
Mol Syst Biol. 2008;4:192. doi: 10.1038/msb.2008.30. Epub 2008 May 6.
9
Macromolecular modeling with rosetta.使用Rosetta进行大分子建模。
Annu Rev Biochem. 2008;77:363-82. doi: 10.1146/annurev.biochem.77.062906.171838.
10
Promiscuous mutations activate the noncanonical NF-kappaB pathway in multiple myeloma.杂乱突变激活多发性骨髓瘤中的非经典核因子κB通路。
Cancer Cell. 2007 Aug;12(2):131-44. doi: 10.1016/j.ccr.2007.07.003.