ArticleMolecular and cellular biology2004
Human immunodeficiency virus type 1 Vpr-mediated G2 arrest requires Rad17 and Hus1 and induces nuclear BRCA1 and gamma-H2AX focus formation.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 118 citations in OpenAlex.
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- BRCA1-RAD51 homologous DNA repair pathway promotes HIV-1 reverse transcription.Science advances · 2026Article
- DNA damage induced by HIV-1 Vpr triggers epigenetic remodeling and transcriptional programs to enhance virus transcription and latency reactivation.PLoS biology · 2026Article
- Review
- Beyond reverse transcription: molecular mechanisms and emerging paradigms in retroviral replication.FEMS microbiology reviews · 2026Review
- Genotoxic consequences of viral infections.Npj viruses · 2025Review
- Oncogenic BRCA1,2 Mutations in the Human Lineage-A By-Product of Sexual Selection?Biomedicines · 2023Review
- Inhibition of ATM-directed antiviral responses by HIV-1 Vif.PLoS pathogens · 2023Article
- Huntingtin-Interacting Protein 1 Promotes Vpr-Induced G2 Arrest and HIV-1 Infection in Macrophages.Viruses · 2021Article
- Predicted Cellular Interactors of the Endogenous Retrovirus-K Integrase Enzyme.Microorganisms · 2021Article
- Article
- HIV-1 and HIV-1-Tat Induce Mitochondrial DNA Damage in Human Neurons.Journal of HIV and AIDS · 2020Article
- Review
- HIV-1 Vpr induces cell cycle arrest and enhances viral gene expression by depleting CCDC137.eLife · 2020Article
- Inflammation-related genes are associated with epigenetic aging in HIV.Journal of neurovirology · 2019Article
- HIV infection and frequency of micronucleus in human peripheral blood cells.Journal of preventive medicine and hygiene · 2019Article
- HIV-1 infection renders brain vascular pericytes susceptible to the extracellular glutamate.Journal of neurovirology · 2019Article
- HIV-1 Vpr Reprograms CLR4mBio · 2018Article
- Structural alteration of DNA induced by viral protein R of HIV-1 triggers the DNA damage response.Retrovirology · 2018Article
- Polyploidy and Mitotic Cell Death Are Two Distinct HIV-1 Vpr-Driven Outcomes in Renal Tubule Epithelial Cells.Journal of virology · 2018Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Eukaryotic cells have evolved a complex mechanism for sensing DNA damage during genome replication. Activation of this pathway prevents entry into mitosis to allow for either DNA repair or, in the event of irreparable damage, commitment to apoptosis. Under conditions of replication stress, the damage signal is initiated by the ataxia-telangiectasia-mutated and Rad3-related kinase ATR. We recently demonstrated that the human immunodeficiency virus type 1 (HIV-1) gene product viral protein R (Vpr) arrests infected cells in the G(2) phase via the activation of ATR. In the present study, we show that the activation of ATR by Vpr is analogous to activation by certain genotoxic agents, both mechanistically and in its downstream consequences. Specifically, we show a requirement for Rad17 and Hus1 to induce G(2) arrest as well as Vpr-induced phosphorylation of histone 2A variant X (H2AX) and formation of nuclear foci containing H2AX and breast cancer susceptibility protein 1. These results demonstrate that G(2) arrest mediated by the HIV-1 gene product Vpr utilizes the cellular signaling pathway whose physiological function is to recognize replication stress. These findings should contribute to a greater understanding of how HIV-1 manipulates the CD4(+)-lymphocyte cell cycle and apoptosis induction in the progressive CD4(+)-lymphocyte depletion characteristic of HIV-1 pathogenesis.
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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.