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N6-甲基腺苷与病毒及病毒诱导疾病的关联。

Association of N6-methyladenosine with viruses and virally induced diseases.

机构信息

Engineering Research Center of Molecular Medicine, Ministry of Education, Huaqiao University, Xiamen, China.

School of Medicine, Huaqiao University, Xiamen, China.

出版信息

Front Biosci (Landmark Ed). 2020 Mar 1;25(6):1184-1201. doi: 10.2741/4852.

DOI:10.2741/4852
PMID:32114429
Abstract

N6-methyladenosine (m6A) modification, which alters gene expression, is the most prevalent internal modification of eukaryotic mRNA. m6A modification is dynamic and reversible that is regulated by three associated protein groups: methyltransferases or writers, demethylases or erasers, and m6A-binding proteins or readers. m6A modification is involved in all phases of RNA life, from RNA folding and structure, stability, splicing, nuclear export, translational modulation to RNA degradation. Recent findings show that the abnormal level of m6A modification causes aberrant expression of important viral genes. Here, we reviewe m6A role in gene expression and its contribution to the development  of human viral diseases. Particularly, we would focus on viruses associated with human diseases including HIV-1, IAV, HBV, HCV, EBV and so on to find a novel approach and provide a new sight for the innovative treatment of human viral diseases.

摘要

N6-甲基腺苷(m6A)修饰改变基因表达,是真核 mRNA 最普遍的内部修饰。m6A 修饰是动态和可逆的,受三个相关蛋白群调控:甲基转移酶或写入器、去甲基酶或橡皮擦,以及 m6A 结合蛋白或读取器。m6A 修饰参与 RNA 生命的所有阶段,从 RNA 折叠和结构、稳定性、剪接、核输出、翻译调节到 RNA 降解。最近的研究结果表明,m6A 修饰水平异常导致重要病毒基因的异常表达。在这里,我们回顾了 m6A 在基因表达中的作用及其对人类病毒性疾病发展的贡献。特别是,我们将重点关注与人类疾病相关的病毒,包括 HIV-1、IAV、HBV、HCV、EBV 等,以寻找新的方法,并为人类病毒性疾病的创新性治疗提供新的视角。

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EMBO J. 2023 Sep 18;42(18):e113378. doi: 10.15252/embj.2022113378. Epub 2023 Jul 11.
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The essential role of N6-methyladenosine RNA methylation in complex eye diseases.
N6-甲基腺苷RNA甲基化在复杂性眼病中的重要作用。
Genes Dis. 2022 May 26;10(2):505-520. doi: 10.1016/j.gendis.2022.05.008. eCollection 2023 Mar.
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Attenuation of IFN signaling due to mA modification of the host epitranscriptome promotes EBV lytic reactivation.宿主转录组 mA 修饰导致 IFN 信号衰减促进 EBV 裂解重新激活。
J Biomed Sci. 2023 Mar 14;30(1):18. doi: 10.1186/s12929-023-00911-9.
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