ArticleeLife2020
HIV-1 Vpr induces cell cycle arrest and enhances viral gene expression by depleting CCDC137.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 82 citations in OpenAlex.
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- CCDC137 affects sorafenib resistance in hepatocellular carcinoma cells by activating the AKT/mTOR signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- A New Type of Nonsuppressible Viremia Produced by HIV-Infected Macrophage.The Journal of infectious diseases · 2026Article
- Article
- DNA damage induced by HIV-1 Vpr triggers epigenetic remodeling and transcriptional programs to enhance virus transcription and latency reactivation.PLoS biology · 2026Article
- CCDC137: A key hub for RNA and epigenetic regulation in cancer research (Review).International journal of oncology · 2026Review
- Under the Radar: Immune Evasion, Pathogenesis and Control of HIV Infection.International journal of molecular sciences · 2025Review
- HIV-1 Vif and Vpr cooperatively modulate the cell cycle to maximize per-cell virion production.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- CCDC137 knockdown suppresses bladder cancer progression by downregulating SCD.Journal of translational medicine · 2025Article
- A New Type of Nonsuppressible Viremia Produced by HIV-Infected Macrophage.bioRxiv : the preprint server for biology · 2025Article
- HIV-1 accessory protein Vpr possesses a cryptic p300-dependent transcription-promoting activity that is blocked by histone deacetylases in CD4+ T cells.PLoS pathogens · 2025Article
- Variation in HIV-1 Tat and Vpr protein amino acid sequences and its association with vascular health measures in a South African cohort: an exploratory study.Virology journal · 2025Article
- Article
- HIV Vpr activates a nucleolar-specific ATR pathway to degrade the nucleolar stress sensor CCDC137.Nucleic acids research · 2025Article
- HIV capsids: orchestrators of innate immune evasion, pathogenesis and pandemicity.The Journal of general virology · 2025Review
- Retrospective analysis of HIV-associated lymphomas: insights from a single Romanian center over 15 years.Frontiers in oncology · 2025Article
- CRL4-DCAF1 Ubiquitin Ligase Dependent Functions of HIV Viral Protein R and Viral Protein X.Viruses · 2024Review
- HIV-1 Vpr combats the PU.1-driven antiviral response in primary human macrophages.Nature communications · 2024Article
- Review
- HIV-1 Vpr Functions in Primary CD4Viruses · 2024Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The HIV-1 Vpr accessory protein induces ubiquitin/proteasome-dependent degradation of many cellular proteins by recruiting them to a cullin4A-DDB1-DCAF1 complex. In so doing, Vpr enhances HIV-1 gene expression and induces (G2/M) cell cycle arrest. However, the identities of Vpr target proteins through which these biological effects are exerted are unknown. We show that a chromosome periphery protein, CCDC137/cPERP-B, is targeted for depletion by HIV-1 Vpr, in a cullin4A-DDB1-DCAF1 dependent manner. CCDC137 depletion caused G2/M cellcycle arrest, while Vpr-resistant CCDC137 mutants conferred resistance to Vpr-induced G2/M arrest. CCDC137 depletion also recapitulated the ability of Vpr to enhance HIV-1 gene expression, particularly in macrophages. Our findings indicate that Vpr promotes cell-cycle arrest and HIV-1 gene expression through depletion of CCDC137.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.