Evidence map›Paper›PMID 22941641›Full record

ArticleNucleic acids research2012

Susceptibility to bystander DNA damage is influenced by replication and transcriptional activity.

Jennifer S Dickey, Brandon J Baird, Christophe E Redon, Valeriya Avdoshina, Guillermo Palchik, Junfang Wu, Alexei Kondratyev, William M Bonner, Olga A Martin

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. NADPH oxidase 4 is a critical mediator in Ataxia telangiectasia disease.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
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

9 authors at 4 institutions in 1 country.

Jennifer S DickeyLaboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20952, USA. Jennifer.Dickey@fda.hhs.gov
Brandon J Baird
Christophe E Redon
Valeriya Avdoshina
Guillermo Palchik
Junfang Wu
Alexei Kondratyev
William M Bonner
Olga A Martin
National Institutes of Health · USCenter for Cancer Research · USDepartment of Health and Human Services · USGeorgetown University Medical Center · US

Funding

Studies of Histone Functions in Chromatin; H2AX and DNA DSBsZIABC006140 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BONNER, WILLIAM · 2009 to 2015
$7.8M
Chromatin Modifications and Vulnerability to Glutamate ToxicityR21NS056057 · NINDS · GEORGETOWN UNIVERSITY · PI KONDRATYEV, ALEXEI D · 2009 to 2010
$422k
Intramural NIH HHSNINDS NIH HHS NS056057
6 · The paper itself

Abstract

Direct cellular DNA damage may lead to genome destabilization in unexposed, bystander, cells sharing the same milieu with directly damaged cells by means of the bystander effect. One proposed mechanism involves double strand break (DSB) formation in S phase cells at sites of single strand lesions in the DNA of replication complexes, which has a more open structure compared with neighboring DNA. The DNA in transcription complexes also has a more open structure, and hence may be susceptible to bystander DSB formation from single strand lesions. To examine whether transcription predisposes non-replicating cells to bystander effect-induced DNA DSBs, we examined two types of primary cells that exhibit high levels of transcription in the absence of replication, rat neurons and human lymphocytes. We found that non-replicating bystander cells with high transcription rates exhibited substantial levels of DNA DSBs, as monitored by γ-H2AX foci formation. Additionally, as reported in proliferating cells, TGF-β and NO were found to mimic bystander effects in cell populations lacking DNA synthesis. These results indicate that cell vulnerability to bystander DSB damage may result from transcription as well as replication. The findings offer insights into which tissues may be vulnerable to bystander genomic destabilization in vivo.

Indexed as

Bystander EffectDNA Breaks, Double-StrandedDNA ReplicationTranscription, GeneticAnimalsBrainCells, CulturedHumansLymphocytesNitric OxideNucleic Acid Synthesis InhibitorsRatsRats, Sprague-DawleyTransforming Growth Factor betaNitric OxideNucleic Acid Synthesis InhibitorsTransforming Growth Factor beta

Identifiers

PMID22941641
PMCPMC3488239
OpenAlexW2028427311

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.