ArticleJournal of virology2007
DDB1 and Cul4A are required for human immunodeficiency virus type 1 Vpr-induced G2 arrest.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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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.
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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
97 citing papers in PubMed.
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- B1486 is a highly potent VprBP inhibitor capable of blocking osteoclast differentiation and bone resorption.The Journal of biological chemistry · 2026Article
- A viral ORFeome library for systems-level genetic dissection of host-pathogen interactions.Cell · 2026Article
- Article
- 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
- CRL4-DCAF1 Ubiquitin Ligase Dependent Functions of HIV Viral Protein R and Viral Protein X.Viruses · 2024Review
- CRL4Life science alliance · 2024Article
- Development of Peptide Displacement Assays to Screen for Antagonists of DDB1 Interactions.Biochemistry · 2024Article
- HIV-1 Vpr Functions in Primary CD4Viruses · 2024Review
- E3 Ubiquitin Ligases in Gammaherpesviruses and HIV: A Review of Virus Adaptation and Exploitation.Viruses · 2023Review
- Discovery of Nanomolar DCAF1 Small Molecule Ligands.Journal of medicinal chemistry · 2023Article
- The CRL4 E3 ligase Mahjong/DCAF1 controls cell competition through the transcription factor Xrp1, independently of polarity genes.Development (Cambridge, England) · 2022Article
- Binding to DCAF1 distinguishes TASOR and SAMHD1 degradation by HIV-2 Vpx.PLoS pathogens · 2021Article
- Article
- xCT/SLC7A11 antiporter function inhibits HIV-1 infection.Virology · 2021Article
- Review
- HIV-1 Vpr induces cell cycle arrest and enhances viral gene expression by depleting CCDC137.eLife · 2020Article
- Review
- Role of the Ubiquitin Proteasome System (UPS) in the HIV-1 Life Cycle.International journal of molecular sciences · 2019Review
- Cellular Cullin RING Ubiquitin Ligases: Druggable Host Dependency Factors of Cytomegaloviruses.International journal of molecular sciences · 2019Review
37 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Vpr-mediated induction of G2 cell cycle arrest has been postulated to be important for human immunodeficiency virus type 1 (HIV-1) replication, but the precise role of Vpr in this cell cycle arrest is unclear. In the present study, we have shown that HIV-1 Vpr interacts with damaged DNA binding protein 1 (DDB1) but not its partner DDB2. The interaction of Vpr with DDB1 was inhibited when DCAF1 (VprBP) expression was reduced by short interfering RNA (siRNA) treatment. The Vpr mutant (Q65R) that was defective for DCAF1 interaction also had a defect in DDB1 binding. However, Vpr binding to DDB1 was not sufficient to induce G2 arrest. A reduction in DDB1 or DDB2 expression in the absence of Vpr also did not induce G2 arrest. On the other hand, Vpr-induced G2 arrest was impaired when the intracellular level of DDB1 or Cullin 4A was reduced by siRNA treatment. Furthermore, Vpr-induced G2 arrest was largely abolished by a proteasome inhibitor. These data suggest that Vpr assembles with DDB1 through interaction with DCAF1 to form an E3 ubiquitin ligase that targets cellular substrates for proteasome-mediated degradation and G2 arrest.
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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.