Ubiquitin-specific Protease 4 Mitigates Toll-like/Interleukin-1 Receptor Signaling and Regulates Innate Immune Activation
Ubiquitin-specific Protease 4 Mitigates Toll-like/Interleukin-1 Receptor Signaling and Regulates Innate Immune Activation
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泛素特异性蛋白酶 4 减轻 Toll 样/白细胞介素 1 受体信号传导并调节先天免疫激活
DOI：
10.1074/jbc.m111.328187
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发表时间：
2012-03-30
影响因子：
4.8
通讯作者：
Zhang, Long
中科院分区：
文献类型：
--
作者：
Zhou, FangFang;Zhang, Xiaofei;Zhang, Long
背景资料：TRAF 6介导的Toll样受体（TLR）/IL-1受体（IL-1 R）通路是先天免疫应答和免疫稳态所必需的。结果：USP 4使TRAF 6的Lys-63连接的多泛素化去泛素化，从而阻止TLR/IL-1 R诱导的NF-κ B和AP-1转录因子的激活以及随后的促炎反应。USP 4在TLR/IL-1 R信号介导的先天免疫应答的负调控中起重要作用。意义：USP 4是一个有吸引力的调节先天免疫应答的新治疗靶点。
Background: The TRAF6-mediated Toll-like receptor (TLR)/IL-1 receptor (IL-1R) pathway is essential for innate immune responses and immune homeostasis.Results: USP4 deubiquitinates Lys-63-linked polyubiquitination of TRAF6 and thereby prevents the TLR/IL-1R-induced activation of NF-kappa B and AP-1 transcription factors and subsequent proinflammatory responses.Conclusion: USP4 plays an essential role in the negative regulation of the TLR/IL-1R signaling-mediated innate immune response.Significance: USP4 is an attractive new therapeutic target for modulation of innate immune responses.