ID1 inhibits foot‐and‐mouth disease virus replication via targeting of interferon pathways
ID1 inhibits foot‐and‐mouth disease virus replication via targeting of interferon pathways
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DOI：
10.1111/febs.15725
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发表时间：
2021-01
期刊：
影响因子：
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通讯作者：
T. Ren;Hao-tai Chen;Xinsheng Liu;Yanxue Wang;Aixia Fan;Linlin Qi;Li Pan;Wenlong Bai;Yongguang Zhang;Yue Sun
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文献类型：
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作者：
T. Ren;Hao-tai Chen;Xinsheng Liu;Yanxue Wang;Aixia Fan;Linlin Qi;Li Pan;Wenlong Bai;Yongguang Zhang;Yue Sun
DNA结合抑制剂1（ID1）蛋白因其在肿瘤发生和维持干细胞样特性中的功能而被广泛研究，但其在病毒感染中的作用却鲜为人知。在本研究中，我们已经清楚地表明，口蹄疫病毒（FMDV）通过Cdh 1介导的泛素化促进ID1降解，以促进其复制。机制研究揭示叉头盒O1（FOXO 1）作为ID1的合作伙伴，它抑制干扰素调节因子3的表达和干扰素（IFN）的生产。进一步的研究发现，ID1通过HDAC4介导的去乙酰化抑制FOXO 1的转录活性，促进IFN的产生和抗病毒免疫应答。这些研究确定了ID1在抑制FDMV复制中的突出作用，这可能扩展到其他病毒。
Inhibitor of DNA‐binding 1 (ID1) protein has been studied intensively for its functions in tumorigenesis and maintenance of stem cell‐like properties, but its roles in virus infection are less understood. In the present study, we have clearly shown that the foot‐and‐mouth disease virus (FMDV) promotes ID1 degradation via Cdh1‐mediated ubiquitination to facilitate its replication. Mechanistic investigations reveal Forkhead Box O1 (FOXO1) as an ID1 partner, which suppresses interferon regulatory factors 3 expression and interferon (IFN) production. Further investigation identified that ID1 suppresses FOXO1 transcription activity through HDAC4‐mediated deacetylation, promoting IFN production and antiviral immune response. These studies establish a prominent role for ID1 in suppressing FDMV replication, which may be extended to other viruses.