• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

莫洛尼白血病病毒 10 型（MOV10）通过干扰 Vif 介导的泛素-蛋白酶体途径抑制 APOBEC3G 的降解。

Moloney leukemia virus 10 (MOV10) inhibits the degradation of APOBEC3G through interference with the Vif-mediated ubiquitin-proteasome pathway.

机构信息

Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.

Key Laboratory of Tropical Disease Control of Ministry of Education, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.

出版信息

Retrovirology. 2017 Dec 19;14(1):56. doi: 10.1186/s12977-017-0382-1.

DOI:10.1186/s12977-017-0382-1
PMID:29258557
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5735797/
Abstract

BACKGROUND

MOV10 protein has ATP-dependent 5'-3' RNA helicase activity and belongs to the UPF1p superfamily. It can inhibit human immunodeficiency virus type 1 (HIV-1) replication at multiple stages and interact with apolipoprotein-B-mRNA-editing enzyme catalytic polypeptide-like 3G (APOBEC3G or A3G), a member of the cytidine deaminase family that exerts potent inhibitory effects against HIV-1 infection. However, HIV-1-encoded virion infectivity factor (Vif) protein specifically mediates the degradation of A3G via the ubiquitin-proteasome system (UPS).

RESULTS

We demonstrate that MOV10 counteracts Vif-mediated degradation of A3G by inhibiting the assembly of the Vif-CBF-β-Cullin 5-ElonginB-ElonginC complex. Through interference with UPS, MOV10 enhances the level of A3G in HIV-1-infected cells and virions, and synergistically inhibits the replication and infectivity of HIV-1. In addition, the DEAG-box of MOV10 is required for inhibition of Vif-mediated A3G degradation as the DEAG-box mutant significantly loses this ability.

CONCLUSIONS

Our results demonstrate a novel mechanism involved in the anti-HIV-1 function of MOV10. Given that both MOV10 and A3G belong to the interferon antiviral system, their synergistic inhibition of HIV-1 suggests that these proteins may play complicated roles in antiviral functions.

摘要

背景

MOV10 蛋白具有 ATP 依赖性 5'-3' RNA 解旋酶活性，属于 UPF1p 超家族。它可以在多个阶段抑制人类免疫缺陷病毒 1 型（HIV-1）的复制，并与载脂蛋白-B-mRNA 编辑酶催化多肽样 3G（APOBEC3G 或 A3G）相互作用，APOBEC3G 是胞苷脱氨酶家族的一员，对 HIV-1 感染具有强大的抑制作用。然而，HIV-1 编码的病毒感染力因子（Vif）蛋白通过泛素-蛋白酶体系统（UPS）特异性介导 A3G 的降解。

结果

我们证明，MOV10 通过抑制 Vif-CBF-β-Cullin 5-ElonginB-ElonginC 复合物的组装来拮抗 Vif 介导的 A3G 降解。通过干扰 UPS，MOV10 增加了 HIV-1 感染细胞和病毒粒子中 A3G 的水平，并协同抑制 HIV-1 的复制和感染性。此外，MOV10 的 DEAG 盒对于抑制 Vif 介导的 A3G 降解是必需的，因为 DEAG 盒突变体显著失去了这种能力。

结论

我们的结果表明，MOV10 具有一种新的抗 HIV-1 功能机制。鉴于 MOV10 和 A3G 均属于干扰素抗病毒系统，它们协同抑制 HIV-1 表明这些蛋白可能在抗病毒功能中发挥复杂作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/e7157dec14e7/12977_2017_382_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/664625f4b5d5/12977_2017_382_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/d6edb2c20a5f/12977_2017_382_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/6762aef17d15/12977_2017_382_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/8905e11996eb/12977_2017_382_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/bce6e42b47f1/12977_2017_382_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/34be2e56e82a/12977_2017_382_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/a5554c936040/12977_2017_382_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/d7f7043bc86c/12977_2017_382_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/19ad66c430bf/12977_2017_382_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/e7157dec14e7/12977_2017_382_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/664625f4b5d5/12977_2017_382_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/d6edb2c20a5f/12977_2017_382_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/6762aef17d15/12977_2017_382_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/8905e11996eb/12977_2017_382_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/bce6e42b47f1/12977_2017_382_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/34be2e56e82a/12977_2017_382_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/a5554c936040/12977_2017_382_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/d7f7043bc86c/12977_2017_382_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/19ad66c430bf/12977_2017_382_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ec/5735797/e7157dec14e7/12977_2017_382_Fig10_HTML.jpg

相似文献

1
Moloney leukemia virus 10 (MOV10) inhibits the degradation of APOBEC3G through interference with the Vif-mediated ubiquitin-proteasome pathway.莫洛尼白血病病毒 10 型（MOV10）通过干扰 Vif 介导的泛素-蛋白酶体途径抑制 APOBEC3G 的降解。
Retrovirology. 2017 Dec 19;14(1):56. doi: 10.1186/s12977-017-0382-1.
2
Characterization of conserved motifs in HIV-1 Vif required for APOBEC3G and APOBEC3F interaction.APOBEC3G和APOBEC3F相互作用所需的HIV-1 Vif中保守基序的特征分析。
J Mol Biol. 2008 Sep 12;381(4):1000-11. doi: 10.1016/j.jmb.2008.06.061. Epub 2008 Jun 28.
3
Translational regulation of APOBEC3G mRNA by Vif requires its 5'UTR and contributes to restoring HIV-1 infectivity.Vif 通过其 5'UTR 对 APOBEC3G mRNA 的翻译调控有助于恢复 HIV-1 感染性。
Sci Rep. 2016 Dec 20;6:39507. doi: 10.1038/srep39507.
4
Identification of a novel HIV-1 inhibitor targeting Vif-dependent degradation of human APOBEC3G protein.一种靶向HIV-1 Vif蛋白介导的人载脂蛋白B mRNA编辑酶催化多肽样3G（APOBEC3G）蛋白降解的新型HIV-1抑制剂的鉴定。
J Biol Chem. 2015 Apr 17;290(16):10504-17. doi: 10.1074/jbc.M114.626903. Epub 2015 Feb 27.
5
A naturally occurring Vif mutant (I107T) attenuates anti-APOBEC3G activity and HIV-1 replication.一种天然存在的 Vif 突变体（I107T）减弱了抗 APOBEC3G 的活性和 HIV-1 的复制。
J Mol Biol. 2013 Aug 23;425(16):2840-52. doi: 10.1016/j.jmb.2013.05.015. Epub 2013 May 23.
6
Differential Contributions of Ubiquitin-Modified APOBEC3G Lysine Residues to HIV-1 Vif-Induced Degradation.泛素修饰的载脂蛋白B mRNA编辑酶催化多肽样蛋白3G（APOBEC3G）赖氨酸残基对HIV-1 Vif诱导降解的不同贡献
J Mol Biol. 2016 Aug 28;428(17):3529-39. doi: 10.1016/j.jmb.2016.05.029. Epub 2016 Jun 10.
7
Inhibition of Vif-Mediated Degradation of APOBEC3G through Competitive Binding of Core-Binding Factor Beta.通过核心结合因子β的竞争性结合抑制Vif介导的载脂蛋白B mRNA编辑酶催化多肽样3G降解
J Virol. 2020 Mar 17;94(7). doi: 10.1128/JVI.01708-19.
8
Small-molecule inhibition of human immunodeficiency virus type 1 replication by targeting the interaction between Vif and ElonginC.小分子通过靶向 Vif 和 ElonginC 之间的相互作用抑制人类免疫缺陷病毒 1 复制。
J Virol. 2012 May;86(10):5497-507. doi: 10.1128/JVI.06957-11. Epub 2012 Feb 29.
9
The HDAC6/APOBEC3G complex regulates HIV-1 infectiveness by inducing Vif autophagic degradation.HDAC6/APOBEC3G复合物通过诱导Vif自噬降解来调节HIV-1的感染性。
Retrovirology. 2015 Jun 24;12:53. doi: 10.1186/s12977-015-0181-5.
10
Mechanism of Enhanced HIV Restriction by Virion Coencapsidated Cytidine Deaminases APOBEC3F and APOBEC3G.病毒体共包装胞苷脱氨酶APOBEC3F和APOBEC3G增强HIV限制的机制
J Virol. 2017 Jan 18;91(3). doi: 10.1128/JVI.02230-16. Print 2017 Feb 1.

引用本文的文献

1
Human microRNA miR-197-3p positively regulates HIV-1 virion infectivity through its target DDX52 by stabilizing Vif protein expression.人类微小RNA miR-197-3p通过稳定Vif蛋白表达，以其靶标DDX52为媒介正向调控HIV-1病毒体的感染性。
J Biol Chem. 2025 Feb;301(2):108198. doi: 10.1016/j.jbc.2025.108198. Epub 2025 Jan 16.
2
Tannic acid reactivates HIV-1 latency by mediating CBX4 degradation.单宁酸通过介导CBX4降解重新激活HIV-1潜伏。
J Virol. 2025 Jan 31;99(1):e0117324. doi: 10.1128/jvi.01173-24. Epub 2024 Dec 18.
3
Recent Insights into the Angioregulatory Role of Long Non-coding RNAs and Circular RNAs in Gliomas: From Signaling Pathways to Clinical Aspects.

本文引用的文献

1
Long noncoding RNA NRON contributes to HIV-1 latency by specifically inducing tat protein degradation.长链非编码 RNA NRON 通过特异性诱导 tat 蛋白降解促进 HIV-1 潜伏。
Nat Commun. 2016 Jun 13;7:11730. doi: 10.1038/ncomms11730.
2
RNA helicase MOV10 functions as a co-factor of HIV-1 Rev to facilitate Rev/RRE-dependent nuclear export of viral mRNAs.RNA解旋酶MOV10作为HIV-1 Rev的辅助因子，促进病毒mRNA依赖Rev/RRE的核输出。
Virology. 2015 Dec;486:15-26. doi: 10.1016/j.virol.2015.08.026. Epub 2015 Sep 14.
3
Identification of an HIV-1 replication inhibitor which rescues host restriction factor APOBEC3G in Vif-APOBEC3G complex.
长链非编码RNA和环状RNA在胶质瘤血管调节作用中的最新见解：从信号通路到临床层面
Curr Med Chem. 2024 Jan 22. doi: 10.2174/0109298673259378231031061149.
4
Unwinding the roles of RNA helicase MOV10.解析RNA解旋酶MOV10的作用
Wiley Interdiscip Rev RNA. 2022 Mar;13(2):e1682. doi: 10.1002/wrna.1682. Epub 2021 Jul 29.
5
Roles of MOV10 in Animal RNA Virus Infection.MOV10在动物RNA病毒感染中的作用。
Front Vet Sci. 2020 Sep 16;7:569737. doi: 10.3389/fvets.2020.569737. eCollection 2020.
6
Inositol-Requiring Enzyme 1α Promotes Zika Virus Infection through Regulation of Stearoyl Coenzyme A Desaturase 1-Mediated Lipid Metabolism.Ins(1,4,5)P3 酶 1α 通过调控硬脂酰辅酶 A 去饱和酶 1 介导的脂代谢促进寨卡病毒感染。
J Virol. 2020 Nov 9;94(23). doi: 10.1128/JVI.01229-20.
7
How HIV-1 Gag Manipulates Its Host Cell Proteins: A Focus on Interactors of the Nucleocapsid Domain.HIV-1 Gag 如何操纵宿主细胞蛋白：重点关注核衣壳域的相互作用蛋白。
Viruses. 2020 Aug 13;12(8):888. doi: 10.3390/v12080888.
8
Hydroxycarboxylic Acid Receptor 2 Is a Zika Virus Restriction Factor That Can Be Induced by Zika Virus Infection Through the IRE1-XBP1 Pathway.羟基羧酸受体 2 是寨卡病毒的限制因子，寨卡病毒感染可以通过 IRE1-XBP1 通路诱导其表达。
Front Cell Infect Microbiol. 2020 Jan 22;9:480. doi: 10.3389/fcimb.2019.00480. eCollection 2019.
9
Strategies for Success. Viral Infections and Membraneless Organelles.成功策略。病毒感染与无膜细胞器。
Front Cell Infect Microbiol. 2019 Oct 11;9:336. doi: 10.3389/fcimb.2019.00336. eCollection 2019.
10
USP49 potently stabilizes APOBEC3G protein by removing ubiquitin and inhibits HIV-1 replication.USP49 通过去除泛素来稳定 APOBEC3G 蛋白，从而抑制 HIV-1 复制。
Elife. 2019 Aug 9;8:e48318. doi: 10.7554/eLife.48318.
鉴定一种 HIV-1 复制抑制剂，该抑制剂可挽救 Vif-APOBEC3G 复合物中的宿主限制因子 APOBEC3G。
Antiviral Res. 2015 Oct;122:20-7. doi: 10.1016/j.antiviral.2015.07.009. Epub 2015 Aug 1.
4
Structure of the Vif-binding domain of the antiviral enzyme APOBEC3G.抗病毒酶载脂蛋白B mRNA编辑酶催化多肽样蛋白3G（APOBEC3G）的Vif结合结构域的结构
Nat Struct Mol Biol. 2015 Jun;22(6):485-91. doi: 10.1038/nsmb.3033. Epub 2015 May 18.
5
Crystal structure of DNA cytidine deaminase ABOBEC3G catalytic deamination domain suggests a binding mode of full-length enzyme to single-stranded DNA.DNA胞苷脱氨酶ABOBEC3G催化脱氨结构域的晶体结构揭示了全长酶与单链DNA的结合模式。
J Biol Chem. 2015 Feb 13;290(7):4010-21. doi: 10.1074/jbc.M114.624262. Epub 2014 Dec 25.
6
Requirement of HIV-1 Vif C-terminus for Vif-CBF-β interaction and assembly of CUL5-containing E3 ligase.HIV-1 Vif C末端对于Vif与CBF-β相互作用及含CUL5的E3连接酶组装的需求
BMC Microbiol. 2014 Nov 26;14:290. doi: 10.1186/s12866-014-0290-7.
7
Determinants of efficient degradation of APOBEC3 restriction factors by HIV-1 Vif.HIV-1 Vif对APOBEC3限制因子高效降解的决定因素。
J Virol. 2014 Dec;88(24):14380-95. doi: 10.1128/JVI.02484-14. Epub 2014 Oct 1.
8
Suppression of APOBEC3-mediated restriction of HIV-1 by Vif.Vif 抑制 APOBEC3 介导的 HIV-1 限制。
Front Microbiol. 2014 Aug 26;5:450. doi: 10.3389/fmicb.2014.00450. eCollection 2014.
9
Identification of HIV-1 Vif regions required for CBF-β interaction and APOBEC3 suppression.鉴定CBF-β相互作用和APOBEC3抑制所需的HIV-1 Vif区域。
PLoS One. 2014 May 8;9(5):e95738. doi: 10.1371/journal.pone.0095738. eCollection 2014.
10
MOV10 Is a 5' to 3' RNA helicase contributing to UPF1 mRNA target degradation by translocation along 3' UTRs.MOV10 是一种 5' 到 3' RNA 解旋酶，通过沿 3'UTR 的易位促进 UPF1mRNA 靶标降解。
Mol Cell. 2014 May 22;54(4):573-85. doi: 10.1016/j.molcel.2014.03.017. Epub 2014 Apr 10.