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首页> 外文期刊>Nature immunology >The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses.
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The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses.

机译：终止Toll样受体反应需要泛素修饰酶A20。

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摘要

A20 is a cytoplasmic protein required for the termination of tumor necrosis factor (TNF)-induced signals. We show here that mice doubly deficient in either A20 and TNF or A20 and TNF receptor 1 developed spontaneous inflammation, indicating that A20 is also critical for the regulation of TNF-independent signals in vivo. A20 was required for the termination of Toll-like receptor-induced activity of the transcription factor NF-kappaB and proinflammatory gene expression in macrophages, and this function protected mice from endotoxic shock. A20 accomplished this biochemically by directly removing ubiquitin moieties from the signaling molecule TRAF6. The critical function of this deubiquitinating enzyme in the restriction of TLR signals emphasizes the importance of the regulation of ubiquitin conjugation in innate immune cells.
机译：A20是终止肿瘤坏死因子（TNF）诱导的信号所需的细胞质蛋白。我们在这里显示，小鼠双倍缺乏A20和TNF或A20和TNF受体1发生自发性炎症，表明A20对于体内不依赖TNF的信号的调节也很关键。 A20是终止Toll样受体诱导的转录因子NF-κB活性和巨噬细胞中促炎基因表达所必需的，该功能可保护小鼠免受内毒素性休克的侵害。 A20通过直接从信号分子TRAF6中去除泛素部分来完成这一生化反应。该去泛素化酶在限制TLR信号中的关键功能强调了先天免疫细胞中泛素结合的调节的重要性。

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