Yersinia YopT inhibits RLH-mediated NF-κB and IRF3 signal transduction
Yersinia YopT inhibits RLH-mediated NF-κB and IRF3 signal transduction
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耶尔森氏菌 YopT 抑制 RLH 介导的 NF-κB 和 IRF3 信号转导。
DOI：
10.1111/1348-0421.12842
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发表时间：
2020-10-19
影响因子：
2.6
通讯作者：
Wei, Congwen
中科院分区：
文献类型：
--
作者：
Li, Dongyu;Wang, Haoyong;Wei, Congwen
革兰氏阴性病原菌耶尔森氏菌将六种效应蛋白递送到宿主细胞中，以阻断宿主的先天免疫反应。其中一种效应蛋白YopT是一种强效的半胱氨酸蛋白酶，它会破坏肌动蛋白细胞骨架，从而抑制病原体的吞噬作用；然而，其分子机制以及与发病机制的相关性需要进一步研究。在本报告中，我们表明RIG - I是YopT蛋白的一个新靶点。值得注意的是，YopT与RIG - I相互作用，并抑制大鼠肝脏匀浆介导的核因子 - κB和干扰素调节因子 - 3的激活。进一步的研究揭示了RIG - I的K48多聚泛素化依赖于YopT而增加。这些发现表明，YopT通过靶向RIG - I负向调节RIG - I介导的细胞抗菌反应。
The Gram-negative bacterial pathogenYersiniadelivers six effector proteins into the host cells to block the host innate immune response. One of the effectors, YopT, is a potent cysteine protease that causes the disruption of the actin cytoskeleton to inhibit phagocytosis of the pathogen; however, its molecular mechanism and relevance to pathogenesis need further investigation. In this report, we show that RIG-I is a novel target of the YopT protein. Remarkably, YopT interacts with RIG-I and inhibits rat liver homogenate-mediated nuclear factor-kappa B and interferon regulatory factor-3 activation. Further studies revealed a YopT-dependent increase in the K48-polymerized ubiquitination of RIG-I. These findings suggest that YopT negatively regulates RIG-I-mediated cellular antibacterial response by targeting RIG-I.