ArticleGenes & development2004
SV40 T antigen interacts with Nbs1 to disrupt DNA replication control.
Article in Genes & development, 2004. 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.
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Who cites it
47 citing papers in PubMed, 88 citations in OpenAlex.
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- 53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).bioRxiv : the preprint server for biology · 2024Article
- Signaling Pathway Alterations Driven by BRCA1 and BRCA2 Germline Mutations are Sufficient to Initiate Breast Tumorigenesis by the PIK3CAH1047R Oncogene.Cancer research communications · 2024Article
- Functional Domains of the Early Proteins and Experimental and Epidemiological Studies Suggest a Role for the Novel Human Polyomaviruses in Cancer.Frontiers in microbiology · 2022Review
- Immortalization of primary sheep embryo kidney cells.In vitro cellular & developmental biology. Animal · 2021Article
- The NS1 protein of the parvovirus MVM Aids in the localization of the viral genome to cellular sites of DNA damage.PLoS pathogens · 2020Article
- Polyploid Giant Cancer Cells, a Hallmark of Oncoviruses and a New Therapeutic Challenge.Frontiers in oncology · 2020Review
- Take your PIKK: tumour viruses and DNA damage response pathways.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Article
- Directed Alternative Splicing in Nijmegen Breakage Syndrome: Proof of Principle Concerning Its Therapeutical Application.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Polyomavirus interaction with the DNA damage response.Virologica Sinica · 2015Review
- Homologous recombination is a primary pathway to repair DNA double-strand breaks generated during DNA rereplication.The Journal of biological chemistry · 2014Article
- Productive replication of human papillomavirus 31 requires DNA repair factor Nbs1.Journal of virology · 2014Article
- Insights into the initiation of JC virus DNA replication derived from the crystal structure of the T-antigen origin binding domain.PLoS pathogens · 2014Article
- Viral interference with DNA repair by targeting of the single-stranded DNA binding protein RPA.PLoS pathogens · 2013Article
- The RING finger protein RNF8 ubiquitinates Nbs1 to promote DNA double-strand break repair by homologous recombination.The Journal of biological chemistry · 2012Article
- Rad50 zinc hook is important for the Mre11 complex to bind chromosomal DNA double-stranded breaks and initiate various DNA damage responses.The Journal of biological chemistry · 2012Article
- Article
- Nuclear IRS-1 and cancer.Journal of cellular physiology · 2012Review
- Design stars: how small DNA viruses remodel the host nucleus.Future virology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nijmegen breakage syndrome (NBS) is characterized by radiation hypersensitivity, chromosomal instability, and predisposition to cancer. Nbs1, the NBS protein, forms a tight complex with Mre11 and Rad50, and these interactions contribute to proper double-strand break repair. The simian virus 40 (SV40) oncoprotein, large T antigen (T), also interacts with Nbs1, and T-containing cells experience chromosomal hyperreplication in a manner dependent on T/Nbs1 complex formation. A substantial fraction of NBS-deficient fibroblasts reinitiate DNA replication in discrete regions, and wild-type Nbs1 corrects this defect. Similarly, synthesis of an N-terminal Nbs1 fragment induced DNA rereplication and tetraploidy, in NBS-deficient but not NBS-proficient cells. Moreover, SV40 origin-containing DNA hyperreplicated in T-containing NBS-deficient cells by comparison with T-containing, Nbs1-reconstituted derivatives. Thus, Nbs1 suppresses rereplication of cellular DNA and SV40 origin-containing replicons, and T targets Nbs1, thereby enhancing the yield of new SV40 genomes during viral DNA replication.
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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.