ArticleVirology2008
Characterization of mre11 loss following HSV-1 infection.
Article in Virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 25 citations in OpenAlex.
- DNA damage responses in HCMV infection: emerging mechanisms and outstanding questions.Journal of virology · 2026Review
- Ubiquitin-specific protease 15 interacts directly with the HSV-1 alkaline nuclease and facilitates viral recombination and replication fork stability.Journal of virology · 2025Article
- Review
- SMC-based immunity against extrachromosomal DNA elements.Biochemical Society transactions · 2023Article
- Pseudorabies Virus Infection Triggers NF-κB Activation via the DNA Damage Response but Actively Inhibits NF-κB-Dependent Gene Expression.Journal of virology · 2021Article
- Herpes Simplex Virus 1 Manipulates Host Cell Antiviral and Proviral DNA Damage Responses.mBio · 2021Article
- ATM-mediated DNA double-strand break response facilitated oncolytic Newcastle disease virus replication and promoted syncytium formation in tumor cells.PLoS pathogens · 2020Article
- Induction of a Cellular DNA Damage Response by Porcine Circovirus Type 2 Facilitates Viral Replication and Mediates Apoptotic Responses.Scientific reports · 2016Article
- H2AX phosphorylation and DNA damage kinase activity are dispensable for herpes simplex virus replication.Virology journal · 2016Article
- HSV-I and the cellular DNA damage response.Future virology · 2015Article
- Structure of the herpes simplex virus 1 genome: manipulation of nicks and gaps can abrogate infectivity and alter the cellular DNA damage response.Journal of virology · 2014Article
- Activation of H2AX and ATM in varicella-zoster virus (VZV)-infected cells is associated with expression of specific VZV genes.Virology · 2014Article
- The HSV-1 exonuclease, UL12, stimulates recombination by a single strand annealing mechanism.PLoS pathogens · 2012Article
- Changing the ubiquitin landscape during viral manipulation of the DNA damage response.FEBS letters · 2011Review
- Bocavirus infection induces a DNA damage response that facilitates viral DNA replication and mediates cell death.Journal of virology · 2011Article
- Physical interaction between the herpes simplex virus type 1 exonuclease, UL12, and the DNA double-strand break-sensing MRN complex.Journal of virology · 2010Article
- Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replication.PLoS pathogens · 2010Article
- The MRN complex in double-strand break repair and telomere maintenance.FEBS letters · 2010Review
- Contributions of nucleotide excision repair, DNA polymerase eta, and homologous recombination to replication of UV-irradiated herpes simplex virus type 1.The Journal of biological chemistry · 2010Article
- Viral manipulation of DNA repair and cell cycle checkpoints.DNA repair · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Herpes simplex virus induces the activation of the cellular DNA double strand break response pathway dependent upon initiation of viral DNA replication. The MRN complex, consisting of Mre11, Rad50 and Nbs1, is an essential component of the DNA double strand break response and other reports have documented its presence at sites of viral DNA replication, interaction with ICP8 and its contribution to efficient viral DNA replication. During our characterization of the DSB response following infection of normal human fibroblasts and telomerase-immortalized keratinocytes, we observed the loss of Mre11 protein at late times following infection. The loss was not dependent upon ICP0, the proteasome or lysosomal protease activity. Like activation of the DSB response pathway, Mre11 loss was prevented under conditions which inhibited viral DNA replication. Analysis of a series of mutant viruses with defects in cleavage and packaging (UL6, UL15, UL17, UL25, UL28, UL32) of viral DNA or in the maturational protease (UL26) failed to identify a viral gene product necessary for Mre11 loss. Inactivation of ATM, a key effector kinase in the DNA double strand break response, had no effect on Mre11 loss and only a moderate effect on HSV yield. Finally, treatment of uninfected cells with the topoisomerase I inhibitor camptothecin, to induce generation of free DNA ends, also resulted in Mre11 loss. These results suggest that Mre11 loss following infection is caused by the generation of free DNA ends during or following viral DNA replication.
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What OpenQuestion holds
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.