揭示新策略:靶向降解 Miz1 以增强对甲型流感病毒的抗病毒防御。

Boyu Xia, Jing Zhao
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引用次数: 0

摘要

泛素系统已被证明在病毒感染期间的免疫反应调控中发挥着重要作用。在最近发表于《科学信号》(Science Signaling)的一篇文章中,Wu 及其同事揭示了转录因子 Miz1 通过招募 HDAC1 至 ifnb1 启动子抑制 I 型干扰素(IFNs)的产生,从而在甲型流感病毒(IAV)感染中发挥促病毒作用。他们的研究表明,一系列 E3 连接酶组合调节 Miz1 的泛素化和降解,并调节 IFNs 的产生和病毒复制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Unraveling Novel Strategies: Targeting Miz1 for Degradation to Enhance Antiviral Defense against Influenza A Virus.

The ubiquitin system has been shown to play an important role in regulation of immune responses during viral infection. In a recent article published in Science Signaling, Wu and colleagues revealed that transcriptional factor Miz1 plays a pro-viral role in influenza A virus (IAV) infection by suppressing type I interferons (IFNs) production through recruiting HDAC1 to ifnb1 promoter. They show that a series of E3 ligases combinatorially regulates Miz1 ubiquitination and degradation and modulates IFNs production and viral replication.

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