ArticleeLife2019
USP49 potently stabilizes APOBEC3G protein by removing ubiquitin and inhibits HIV-1 replication.
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Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23citing papers in PubMed
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23 citing papers in PubMed, 32 citations in OpenAlex.
- Methaneseleninic acid, a circadian-modulating agent, reactivates latent HIV-1 infection without cellular activation or proliferation.Journal of virology · 2026Article
- The Deubiquitinase OTUD1 Influences HIV-1 Release by Regulating the Host Restriction Factor BST-2.Viruses · 2025Article
- APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction.International journal of molecular sciences · 2025Review
- DCAF13-mediated K63-linked ubiquitination of RNA polymerase I promotes uncontrolled proliferation in Breast Cancer.Nature communications · 2025Article
- FBXO2 promotes hepatocellular carcinoma progression and sorafenib resistance by targeting USP49 for proteasomal degradation.Frontiers in immunology · 2025Article
- Ectopic USP15 expression inhibits HIV-1 transcription involving changes in YY1 deubiquitination and stability.Frontiers in cellular and infection microbiology · 2024Article
- The Involvement of Ubiquitination and SUMOylation in Retroviruses Infection and Latency.Viruses · 2023Review
- USP49 deubiquitinase regulates the mitotic spindle checkpoint and prevents aneuploidy.Cell death & disease · 2023Article
- FBXO34 promotes latent HIV-1 activation by post-transcriptional modulation.Emerging microbes & infections · 2022Article
- USP49 mediates tumor progression and poor prognosis through a YAP1-dependent feedback loop in gastric cancer.Oncogene · 2022Article
- Fbxo45 facilitates pancreatic carcinoma progression by targeting USP49 for ubiquitination and degradation.Cell death & disease · 2022Article
- Review
- Broadly neutralizing antibody-derived CAR T cells reduce viral reservoir in individuals infected with HIV-1.The Journal of clinical investigation · 2021Article
- Long non-coding RNA NEAT1 facilitates the growth, migration, and invasion of ovarian cancer cells via the let-7 g/MEST/ATGL axis.Cancer cell international · 2021Article
- Deubiquitinating Enzyme USP21 Inhibits HIV-1 Replication by Downregulating Tat Expression.Journal of virology · 2021Article
- The interferon-stimulated exosomal hACE2 potently inhibits SARS-CoV-2 replication through competitively blocking the virus entry.Signal transduction and targeted therapy · 2021Article
- Role of Virally-Encoded Deubiquitinating Enzymes in Regulation of the Virus Life Cycle.International journal of molecular sciences · 2021Review
- KDM4C contributes to cytarabine resistance in acute myeloid leukemiaTherapeutic advances in chronic disease · 2021Article
- Specific Deubiquitinating Enzymes Promote Host Restriction Factors Against HIV/SIV Viruses.Frontiers in immunology · 2021Article
- Role of Host-Mediated Post-Translational Modifications (PTMs) in RNA Virus Pathogenesis.International journal of molecular sciences · 2020Review
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Authors and funding
22 authors at 2 institutions in 1 country.
Ting PanInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.ORCID 0000-0002-7106-7312
Zheng SongInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Liyang WuInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Guangyan LiuInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.ORCID 0000-0002-5891-1830
Xiancai MaInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.ORCID 0000-0002-4934-4221
Zhilin PengInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Mo ZhouInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Liting LiangInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Bingfeng LiuInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Jun LiuInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Junsong ZhangInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Xuanhong ZhangInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Ryan HuangInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Jiacong ZhaoInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Yonghong LiInfectious Disease Center, Guangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, China.
Xuemei LingInfectious Disease Center, Guangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, China.
Yuewen LuoInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Xiaoping TangInfectious Disease Center, Guangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, China.
Weiping CaiInfectious Disease Center, Guangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, China.
Kai DengInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Linghua LiInfectious Disease Center, Guangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, China.
Hui ZhangInstitute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.ORCID 0000-0003-3620-610X
Sun Yat-sen University · CNGuangzhou Eighth People's Hospital · CN
Funding
National Natural Science Foundation of China 8197080527National Natural Science Foundation of China 81971918National Natural Science Foundation of China Key Program 81730060National Special Research Program of China for Important Infectious Diseases 2017ZX10202102National Special Research Program of China for Important Infectious Diseases 2018ZX10302103National Special Research Program of China for Important Infectious Diseases 2018ZX10302103; 2017ZX10202102Pearl River S and T Nova Program of Guangzhou 201806010118The Important Key Program of the Natural Science Foundation of China 81730060The International Collaboration Program of the Natural Science Foundation of China and the U.S. NIH 81561128007The International Collaboration Program of the Natural Science Foundation of China and the US NIH 81561128007The Joint-Innovation Program in Healthcare for Special Scientific Research Projects of Guangzhou 201803040002The Science and Technology Planning Project of Guangzhou 201704020226
Abstract
The antiviral activity of host factor apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G (APOBEC3G, A3G) and its degradation mediated by human immunodeficiency virus type 1 (HIV-1) Vif protein are important topics. Although accumulating evidence indicates the importance of deubiquitination enzymes (DUBs) in innate immunity, it is unknown if they participate in A3G stability. Here, we found that USP49 directly interacts with A3G and efficiently removes ubiquitin, consequently increasing A3G protein expression and significantly enhancing its anti-HIV-1 activity. Unexpectedly, A3G degradation was also mediated by a Vif- and cullin-ring-independent pathway, which was effectively counteracted by USP49. Furthermore, clinical data suggested that USP49 is correlated with A3G protein expression and hypermutations in Vif-positive proviruses, and inversely with the intact provirus ratio in the HIV-1 latent reservoir. Our studies demonstrated a mechanism to effectively stabilize A3G expression, which could comprise a target to control HIV-1 infection and eradicate the latent reservoir.
Indexed as
Virus ReplicationAPOBEC-3G DeaminaseHEK293 CellsHeLa CellsHIV-1HumansImmunity, InnateImmunologic FactorsUbiquitinUbiquitin ThiolesteraseAPOBEC-3G DeaminaseAPOBEC3G protein, humanImmunologic FactorsUbiquitinUbiquitin ThiolesteraseUSP49 protein, humanAPOBEC3GdeubiquitinationHIV-1infectious diseasemicrobiologyUSP49Vifvirus
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