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探索新策略:靶向Miz1进行降解以增强抗甲型流感病毒的抗病毒防御

Unraveling Novel Strategies: Targeting Miz1 for Degradation to Enhance Antiviral Defense against Influenza A Virus.

作者信息

Xia Boyu, Zhao Jing

机构信息

Department of Physiology and Cell Biology, Dorothy M. Davis Heart and Lung Research Institute, Columbus, OH 43210, USA.

Department of Internal Medicine, The Ohio State University, Columbus, OH 43210, USA.

出版信息

J Respir Biol Transl Med. 2024 Jun;1(2). doi: 10.35534/jrbtm.2024.10009. Epub 2024 Jun 17.

Abstract

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.

摘要

泛素系统已被证明在病毒感染期间的免疫反应调节中发挥重要作用。在最近发表于《科学信号》的一篇文章中,吴等人揭示转录因子Miz1在甲型流感病毒(IAV)感染中发挥促病毒作用,它通过招募HDAC1至ifnb1启动子来抑制I型干扰素(IFN)的产生。他们表明一系列E3连接酶联合调节Miz1的泛素化和降解,并调节IFN的产生和病毒复制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d631/11290323/54c83fb8d348/nihms-2002985-f0001.jpg

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