NF-κB-mediated degradation of the coactivator RIP140 regulates inflammatory responses and contributes to endotoxin tolerance

HoP.-C.; TsuiY.-C.; FengX.; GreavesD.R.; WeiL.-N.

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NF-κB-mediated degradation of the coactivator RIP140 regulates inflammatory responses and contributes to endotoxin tolerance

机译：NF-κB介导的共激活因子RIP140的降解调节炎症反应并有助于内毒素耐受

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Tolerance to endotoxins that is triggered by prior exposure to Toll-like receptor (TLR) ligands provides a mechanism with which to dampen inflammatory cytokines. The receptor-interacting protein RIP140 interacts with the transcription factor NF-κB to regulate the expression of genes encoding proinflammatory cytokines. Here we found lipopolysaccharide stimulation of kinase Syk-mediated tyrosine phosphorylation of RIP140 and interaction of the NF-κB subunit RelA with RIP140. These events resulted in more recruitment of the E3 ligase SCF to tyrosine-phosphorylated RIP140, which degraded RIP140 to inactivate genes encoding inflammatory cytokines. Macrophages expressing nondegradable RIP140 were resistant to the establishment of endotoxin tolerance for specific 'tolerizable' genes. Our results identify RelA as an adaptor with which SCF fine tunes NF-κB target genes by targeting the coactivator RIP140 and show an unexpected role for RIP140 degradation in resolving inflammation and endotoxin tolerance.

机译：事先暴露于Toll样受体（TLR）配体引起的对内毒素的耐受性提供了一种抑制炎症细胞因子的机制。受体相互作用蛋白RIP140与转录因子NF-κB相互作用，以调节编码促炎细胞因子的基因的表达。在这里，我们发现脂多糖刺激激酶Syk介导的RIP140的酪氨酸磷酸化以及NF-κB亚基RelA与RIP140的相互作用。这些事件导致更多的E3连接酶SCF募集到酪氨酸磷酸化的RIP140，从而使RIP140降解以使编码炎症细胞因子的基因失活。表达不可降解RIP140的巨噬细胞对内毒素对特定“可耐受”基因的耐受性具有抗性。我们的结果确定RelA为SCF通过靶向共激活因子RIP140来微调NF-κB靶基因的衔接子，并显示RIP140降解在解决炎症和内毒素耐受性方面具有意想不到的作用。

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《Nature immunology》 |2012年第4期|共8页
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HoP.-C.; TsuiY.-C.; FengX.; GreavesD.R.; WeiL.-N.;
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1. NF-κB-mediated degradation of the coactivator RIP140 regulates inflammatory responses and contributes to endotoxin tolerance [J] . HoP.-C., TsuiY.-C., FengX., Nature immunology . 2012,第4期

机译：NF-κB介导的共激活因子RIP140的降解调节炎症反应并有助于内毒素耐受
2. Inflammatory responses associated with acute coronary syndrome up-regulate IRAK-M and induce endotoxin tolerance in circulating monocytes. [J] . del-Fresno C, Soler-Rangel L, Soares-Schanoski A, Journal of endotoxin research . 2007,第1期

机译：与急性冠状动脉综合征相关的炎症反应上调IRAK-M并诱导循环单核细胞对内毒素的耐受。
3. Ubiquitin-Fold Modifier-1 Participates in the Diabetic Inflammatory Response by Regulating NF-κB p65 Nuclear Translocation and the Ubiquitination and Degradation of IκBα [J] . Xiaolei Hu, Hengyan Zhang, Langen Zhuang, Drug Design, Development and Therapy . 2020,第1期

机译：泛素折叠改性剂-1通过调节NF-κBP65核转位和IκBα的泛素化和降解来参与糖尿病炎症反应
4. HDL3 protects vascular endothelial cells from lipopolysaccharide- induced injure by inhibiting the NF-κB-mediated inflammatory reaction [C] . Hui Sang, Shutong Yao, Linlin Gao, International Symposium on Information Technologies in Medicine and Education;ITME 2012 . 2012

机译：HDL3通过抑制NF-κB介导的炎症反应来保护血管内皮细胞免受脂多糖诱导的损伤
5. Functional role of receptor-interacting protein 140 (RIP140) in adipocyte dysfunctions and inflammatory response in macrophages [D] . Ho, Ping-Chih 2012

机译：受体相互作用蛋白140（RIP140）在脂肪细胞功能障碍和巨噬细胞炎症反应中的功能作用
6. NF-κB-mediated degradation of the co-activator RIP140 regulates inflammatory response and contributes to endotoxin tolerance [O] . Ping-Chih Ho, Yao-Chen Tsui, Xudong Feng, -1

机译：共活化剂的NF-κB介导的降解RIp140调节炎症反应并有助于内毒素耐受
7. NF-κB-mediated degradation of the coactivator RIP140 regulates inflammatory responses and contributes to endotoxin tolerance. [O] . Ho, PC, Tsui, YC, Feng, X, 2012

机译：NF-κB介导的共激活因子RIP140的降解调节炎症反应并有助于内毒素耐受。

NF-κB-mediated degradation of the coactivator RIP140 regulates inflammatory responses and contributes to endotoxin tolerance

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