Mst1 shuts off cytosolic antiviral defense through IRF3 phosphorylation.
Mst1 shuts off cytosolic antiviral defense through IRF3 phosphorylation.
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Mst1 通过 IRF3 磷酸化关闭胞质抗病毒防御
DOI：
10.1101/gad.277533.116
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发表时间：
2016-05-01
影响因子：
10.5
通讯作者：
Xu P
中科院分区：
文献类型：
--
作者：
Meng F;Zhou R;Wu S;Zhang Q;Jin Q;Zhou Y;Plouffe SW;Liu S;Song H;Xia Z;Zhao B;Ye S;Feng XH;Guan KL;Zou J;Xu P
在这里，Meng等人研究了干扰素调节因子3（IRF 3）激活（抗病毒传感途径的关键信号介体/转录因子）是如何调节的。他们证明，Mst 1是一种应激反应激酶，通过抑制RNA病毒诱导的TBK 1活化和干扰IRF 3同源二聚化以及通过IRF 3 Thr 253和Thr 75残基的直接磷酸化与染色质结合来抑制胞质抗病毒传感和防御。
Here, Meng et al. investigated how interferon regulatory factor 3 (IRF3) activation, a key signal mediator/transcriptional factor of the antiviral-sensing pathway, is regulated. They demonstrate that Mst1, a stress response kinase, represses cytosolic antiviral sensing and defense through the repression of RNA virus-induced activation of TBK1 and interference with the IRF3 homodimerization and chromatin binding via direct phosphorylation of IRF3 Thr253 and Thr75 residues.