Evidence map›Paper›PMID 20519379›Full record

ArticleJournal of virology2010

Multiple DNA damage signaling and repair pathways deregulated by simian virus 40 large T antigen.

Sergei Boichuk, Liang Hu, Jennifer Hein, Ole V Gjoerup

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

64 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
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  3. Review
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  5. Review
  6. Unlicensed origin DNA melting by MCV and SV40 polyomavirus LT proteins is independent of ATP-dependent helicase activity.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  9. Article
  10. Review
  11. Article
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  14. Review
  15. Checkpoint inhibitor blockade and epigenetic reprogrammability in CD8Therapeutic advances in vaccines and immunotherapy · 2020
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Sergei BoichukUniversity of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania 15213, USA.
Liang Hu
Jennifer Hein
Ole V Gjoerup
UPMC Hillman Cancer Center · US

Funding

Role of Bub1 in SV40 large T antigen mediated transformation and replicationR01AI078926 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GJOERUP, OLE · 2008 to 2011
$1.5M
NIAID NIH HHS R01 AI078926NIAID NIH HHS R01AI078926NIGMS NIH HHS GM07166
6 · The paper itself

Abstract

We demonstrated previously that expression of simian virus 40 (SV40) large T antigen (LT), without a viral origin, is sufficient to induce the hallmarks of a cellular DNA damage response (DDR), such as focal accumulation of gamma-H2AX and 53BP1, via Bub1 binding. Here we expand our characterization of LT effects on the DDR. Using comet assays, we demonstrate that LT induces overt DNA damage. The Fanconi anemia pathway, associated with replication stress, becomes activated, since FancD2 accumulates in foci, and monoubiquitinated FancD2 is detected on chromatin. LT also induces a distinct set of foci of the homologous recombination repair protein Rad51 that are colocalized with Nbs1 and PML. The FancD2 and Rad51 foci require neither Bub1 nor retinoblastoma protein binding. Strikingly, wild-type LT is localized on chromatin at, or near, the Rad51/PML foci, but the LT mutant in Bub1 binding is not localized there. SV40 infection was previously shown to trigger ATM activation, which facilitates viral replication. We demonstrate that productive infection also triggers ATR-dependent Chk1 activation and that Rad51 and FancD2 colocalize with LT in viral replication centers. Using small interfering RNA (siRNA)-mediated knockdown, we demonstrate that Rad51 and, to a lesser extent, FancD2 are required for efficient viral replication in vivo, suggesting that homologous recombination is important for high-level extrachromosomal replication. Taken together, the interplay of LT with the DDR is more complex than anticipated, with individual domains of LT being connected to different subcomponents of the DDR and repair machinery.

Indexed as

DNA DamageDNA RepairHost-Pathogen InteractionsAnimalsAntigens, Viral, TumorCell Cycle ProteinsCells, CulturedCheckpoint Kinase 1ChromatinComet AssayFanconi Anemia Complementation Group D2 ProteinGene SilencingHaplorhiniHumansModels, BiologicalNuclear ProteinsAntigens, Viral, TumorCell Cycle ProteinsCheckpoint Kinase 1CHEK1 protein, humanChromatinFanconi Anemia Complementation Group D2 ProteinNBN protein, humanNuclear ProteinsPML protein, humanPromyelocytic Leukemia ProteinProtein KinasesRad51 RecombinaseTranscription FactorsTumor Suppressor ProteinsVirulence Factors

Identifiers

PMID20519379
PMCPMC2916509
OpenAlexW2131268542

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.