ArticleJournal of virology2006
Phosphorylation of MCM4 at sites inactivating DNA helicase activity of the MCM4-MCM6-MCM7 complex during Epstein-Barr virus productive replication.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 62 citations in OpenAlex.
- Modulation of DNA Damage by Epstein-Barr Virus (EBV).Viruses · 2026Review
- Identification of a New Phosphorylated Host Interactor of the Epstein-Barr Virus (EBV) Kinase BGLF4 Suggests Key Points for EBV-Specific Antiviral Drug Targeting.International journal of molecular sciences · 2026Article
- Identification of viral activators of the HSV-2 UL13 protein kinase.Journal of virology · 2025Article
- Regulatory mimicry of cyclin-dependent kinases by a conserved herpesvirus protein kinase.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A thorough insight into the life cycle of the Epstein-Barr virus. From the molecular to the organismal level.Current research in microbial sciences · 2025Review
- Multi-omics pan-cancer analyses identify MCM4 as a promising prognostic and diagnostic biomarker.Scientific reports · 2024Article
- ATM, KAP1 and the Epstein-Barr virus polymerase processivity factor direct traffic at the intersection of transcription and replication.Nucleic acids research · 2023Article
- Replication Compartments-The Great Survival Strategy for Epstein-Barr Virus Lytic Replication.Microorganisms · 2022Review
- Biochemical characterization of Plasmodium falciparum parasite specific helicase 1 (PfPSH1).FEBS open bio · 2019Article
- Conserved Herpesvirus Protein Kinases Target SAMHD1 to Facilitate Virus Replication.Cell reports · 2019Article
- Post-Translational Modifications of the Mini-Chromosome Maintenance Proteins in DNA Replication.Genes · 2019Review
- Kaposi's Sarcoma-Associated Herpesvirus Deregulates Host Cellular Replication during Lytic Reactivation by Disrupting the MCM Complex through ORF59.Journal of virology · 2018Article
- Regulation of Herpes Simplex Virus 2 Protein Kinase UL13 by Phosphorylation and Its Role in Viral Pathogenesis.Journal of virology · 2018Article
- Role of MCM2-7 protein phosphorylation in human cancer cells.Cell & bioscience · 2018Review
- Herpes simplex virus-1 evasion of CD8+ T cell accumulation contributes to viral encephalitis.The Journal of clinical investigation · 2017Article
- Potent DNA strand annealing activity associated with mouse Mcm2∼7 heterohexameric complex.Nucleic acids research · 2017Article
- Phosphoproteomic Profiling Reveals Epstein-Barr Virus Protein Kinase Integration of DNA Damage Response and Mitotic Signaling.PLoS pathogens · 2015Article
- BGLF4 kinase modulates the structure and transport preference of the nuclear pore complex to facilitate nuclear import of Epstein-Barr virus lytic proteins.Journal of virology · 2015Article
- A locus encompassing the Epstein-Barr virus bglf4 kinase regulates expression of genes encoding viral structural proteins.PLoS pathogens · 2014Article
- DNA virus replication compartments.Journal of virology · 2014Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Induction of Epstein-Barr virus (EBV) lytic replication blocks chromosomal DNA replication notwithstanding an S-phase-like cellular environment with high cyclin-dependent kinase (CDK) activity. We report here that the phosphorylated form of MCM4, a subunit of the MCM complex essential for chromosomal DNA replication, increases with progression of lytic replication, Thr-19 and Thr-110 being CDK2/CDK1 targets whose phosphorylation inactivates MCM4-MCM6-MCM7 (MCM4-6-7) complex-associated DNA helicase. Expression of EBV-encoded protein kinase (EBV-PK) in HeLa cells caused phosphorylation of these sites on MCM4, leading to cell growth arrest. In vitro, the sites of MCM4 of the MCM4-6-7 hexamer were confirmed to be phosphorylated with EBV-PK, with the same loss of helicase activity as with CDK2/cyclin A. Introducing mutations in the N-terminal six Ser and Thr residues of MCM4 reduced the inhibition by CDK2/cyclin A, while EBV-PK inhibited the helicase activities of both wild-type and mutant MCM4-6-7 hexamers, probably since EBV-PK can phosphorylate MCM6 and another site(s) of MCM4 in addition to the N-terminal residues. Therefore, phosphorylation of the MCM complex by redundant actions of CDK and EBV-PK during lytic replication might provide one mechanism to block chromosomal DNA replication in the infected cells through inactivation of DNA unwinding by the MCM4-6-7 complex.
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