ArticleJournal of virology2008
Differential requirements of the C terminus of Nbs1 in suppressing adenovirus DNA replication and promoting concatemer formation.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 58 citations in OpenAlex.
- Association of hepatitis B virus genomes with active chromatin hubs challenges host replication fidelity, leading to DNA damage.Journal of virology · 2025Article
- Adeno-Associated Virus 2 (AAV2) - Induced RPA exhaustion generates cellular DNA damage and restricts viral gene expression.PLoS pathogens · 2025Article
- Cellular transcription factor TFII-I represses adenovirus gene expression.Journal of virology · 2025Article
- The immediate-early protein 1 of human herpesvirus 6B interacts with NBS1 and inhibits ATM signaling.EMBO reports · 2024Article
- Identification of Adenovirus E1B-55K Interaction Partners through a Common Binding Motif.Viruses · 2023Article
- Viral Modulation of the DNA Damage Response and Innate Immunity: Two Sides of the Same Coin.Journal of molecular biology · 2022Review
- Utilization of Host Cell Chromosome Conformation by Viral Pathogens: Knowing When to Hold and When to Fold.Frontiers in immunology · 2021Review
- Review
- Review
- Repair of protein-linked DNA double strand breaks: Using the adenovirus genome as a model substrate in cell-based assays.DNA repair · 2019Article
- Article
- Ubiquitination at the interface of tumor viruses and DNA damage responses.Current opinion in virology · 2018Review
- Virus DNA Replication and the Host DNA Damage Response.Annual review of virology · 2018Review
- Serotype-specific restriction of wild-type adenoviruses by the cellular Mre11-Rad50-Nbs1 complex.Virology · 2018Article
- The Development of Oncolytic Adenovirus Therapy in the Past and Future - For the Case of Pancreatic CancerCurrent cancer drug targets · 2018Review
- Identifying Host Factors Associated with DNA Replicated During Virus Infection.Molecular & cellular proteomics : MCP · 2017Article
- Review
- Take your PIKK: tumour viruses and DNA damage response pathways.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Adenovirus Core Protein VII Downregulates the DNA Damage Response on the Host Genome.Journal of virology · 2017Article
- Normal human cell proteins that interact with the adenovirus type 5 E1B 55kDa protein.Virology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Adenoviruses (Ad) with the early region E4 deleted (E4-deleted virus) are defective for DNA replication and late protein synthesis. Infection with E4-deleted viruses results in activation of a DNA damage response, accumulation of cellular repair factors in foci at viral replication centers, and joining together of viral genomes into concatemers. The cellular DNA repair complex composed of Mre11, Rad50, and Nbs1 (MRN) is required for concatemer formation and full activation of damage signaling through the protein kinases Ataxia-telangiectasia mutated (ATM) and ATM-Rad3-related (ATR). The E4orf3 and E4orf6 proteins expressed from the E4 region of Ad type 5 (Ad5) inactivate the MRN complex by degradation and mislocalization, and prevent the DNA damage response. Here we investigated individual contributions of the MRN complex, concatemer formation, and damage signaling to viral DNA replication during infection with E4-deleted virus. Using virus mutants, short hairpin RNA knockdown and hypomorphic cell lines, we show that inactivation of MRN results in increased viral replication. We demonstrate that defective replication in the absence of E4 is not due to concatemer formation or DNA damage signaling. The C terminus of Nbs1 is required for the inhibition of Ad DNA replication and recruitment of MRN to viral replication centers. We identified regions of Nbs1 that are differentially required for concatemer formation and inhibition of Ad DNA replication. These results demonstrate that targeting of the MRN complex explains the redundant functions of E4orf3 and E4orf6 in promoting Ad DNA replication. Understanding how MRN impacts the adenoviral life cycle will provide insights into the functions of this DNA damage sensor.
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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.