ArticleThe Journal of biological chemistry2010
Large T antigen promotes JC virus replication in G2-arrested cells by inducing ATM- and ATR-mediated G2 checkpoint signaling.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 80 citations in OpenAlex.
- Human glial chimeric mice reveal astrocytic dependence of JC virus infection.The Journal of clinical investigation · 2014Trial
- John Cunningham Virus and Colorectal Carcinogenesis: Current Evidence, Molecular Mechanisms, and Unresolved Controversies.Reviews in medical virology · 2026Review
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- Genotoxic Bacteria and Oncogenic Viruses in Colorectal Cancer: Evidence, Gaps, and a Proposed Interaction Model.International journal of molecular sciences · 2026Review
- Causal Links Between Antibody-Mediated Immune Responses and Pancreatic Cancer Risk.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Investigation of mRNA expression levels of DNA damage response genes in Merkel Cell Polyomavirus-positive Merkel Cell Carcinoma: a pilot study.Discover oncology · 2025Article
- JC virus spread is potentiated by glial replication and demyelination-linked glial proliferation.Brain : a journal of neurology · 2024Article
- Prevalence of BK and JC Polyomaviruses among Patients with Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- Single-Cell, High-Content Microscopy Analysis of BK Polyomavirus Infection.Microbiology spectrum · 2023Article
- DNA Damage Response Differentially Affects BoHV-1 Gene Transcription in Cell Type-Dependent Manners.Biomedicines · 2022Article
- BK Polyomavirus Requires the Mismatch Repair Pathway for DNA Damage Response Activation.Journal of virology · 2022Article
- Viruses in colorectal cancer.Molecular oncology · 2022Review
- Virus-host interaction analysis in colorectal cancer identifies core virus network signature and small molecules.Computational and structural biotechnology journal · 2022Article
- The oncogenic roles of JC polyomavirus in cancer.Frontiers in oncology · 2022Review
- RNA Sequencing of Medusavirus Suggests Remodeling of the Host Nuclear Environment at an Early Infection Stage.Microbiology spectrum · 2021Article
- Chk1 and the Host Cell DNA Damage Response as a Potential Antiviral Target in BK Polyomavirus Infection.Viruses · 2021Article
- Review
- Murine polyomavirus DNA transitions through spatially distinct nuclear replication subdomains during infection.PLoS pathogens · 2020Article
- Microtubules in Polyomavirus Infection.Viruses · 2020Review
- Temporal Proteomic Analysis of BK Polyomavirus Infection Reveals Virus-Induced GJournal of virology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Large T antigen (TAg) of the human polyomavirus JC virus (JCV) possesses DNA binding and helicase activities, which, together with various cellular proteins, are required for replication of the viral genome. We now show that JCV-infected cells expressing TAg accumulate in the G(2) phase of the cell cycle as a result of the activation of ATM- and ATR-mediated G(2) checkpoint pathways. Transient transfection of cells with a TAg expression vector also induced G(2) checkpoint signaling and G(2) arrest. Analysis of TAg mutants with different subnuclear localizations suggested that the association of TAg with cellular DNA contributes to the induction of G(2) arrest. Abrogation of G(2) arrest by inhibition of ATM and ATR, Chk1, and Wee1 suppressed JCV genome replication. In addition, abrogation of the G(2)-M transition by Cdc2 depletion disabled Wee1 depletion-induced suppression of JCV genome replication, suggesting that JCV replication is facilitated by G(2) arrest resulting from G(2) checkpoint signaling. Moreover, inhibition of ATM and ATR by caffeine suppressed JCV production. The observation that oligodendrocytes productively infected with JCV in vivo also undergo G(2) arrest suggests that G(2) checkpoint inhibitors such as caffeine are potential therapeutic agents for JCV infection.
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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.