ArticlePLoS pathogens2013
Viral interference with DNA repair by targeting of the single-stranded DNA binding protein RPA.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Genomes of the autonomous parvovirus minute virus of mice induce replication stress through RPA exhaustion.PLoS pathogens · 2023Article
- Emetine in Combination with Chloroquine Induces Oncolytic Potential of HIV-1-Based Lentiviral Particles.Cells · 2022Article
- Article
- Human polyomavirus modulation of the host DNA damage response.Virus genes · 2020Review
- Murine polyomavirus DNA transitions through spatially distinct nuclear replication subdomains during infection.PLoS pathogens · 2020Article
- Checkpoint inhibitor blockade and epigenetic reprogrammability in CD8Therapeutic advances in vaccines and immunotherapy · 2020Review
- Article
- Viral DNA replication-dependent DNA damage response activation during BK polyomavirus infection.Journal of virology · 2015Article
- Polyomavirus interaction with the DNA damage response.Virologica Sinica · 2015Review
- SV40 utilizes ATM kinase activity to prevent non-homologous end joining of broken viral DNA replication products.PLoS pathogens · 2014Article
- The "histone mimicry" by pathogens.Cold Spring Harbor symposia on quantitative biology · 2013Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Correct repair of damaged DNA is critical for genomic integrity. Deficiencies in DNA repair are linked with human cancer. Here we report a novel mechanism by which a virus manipulates DNA damage responses. Infection with murine polyomavirus sensitizes cells to DNA damage by UV and etoposide. Polyomavirus large T antigen (LT) alone is sufficient to sensitize cells 100 fold to UV and other kinds of DNA damage. This results in activated stress responses and apoptosis. Genetic analysis shows that LT sensitizes via the binding of its origin-binding domain (OBD) to the single-stranded DNA binding protein replication protein A (RPA). Overexpression of RPA protects cells expressing OBD from damage, and knockdown of RPA mimics the LT phenotype. LT prevents recruitment of RPA to nuclear foci after DNA damage. This leads to failure to recruit repair proteins such as Rad51 or Rad9, explaining why LT prevents repair of double strand DNA breaks by homologous recombination. A targeted intervention directed at RPA based on this viral mechanism could be useful in circumventing the resistance of cancer cells to therapy.
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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.