Evidence map›Paper›PMID 18367668›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2008

Defective p53 engagement after the induction of DNA damage in cells deficient in topoisomerase 3beta.

Subhasis Mohanty, Terrence Town, Tomohito Yagi, Christina Scheidig, Kelvin Y Kwan, Heather G Allore, Richard A Flavell, Albert C Shaw

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. The Roles of Topoisomerases in Transcriptional Regulation.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Article
  4. The many lives of type IA topoisomerases.The Journal of biological chemistry · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Trypanosomatids topoisomerase re-visited. New structural findings and role in drug discovery.International journal for parasitology. Drugs and drug resistance · 2014
    Review
  11. Article
  12. 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

8 authors at 3 institutions in 1 country.

Subhasis MohantySection of Infectious Diseases, Departments of Internal Medicine and Immunobiology, Yale University School of Medicine, New Haven, CT 06520.
Terrence Town
Tomohito Yagi
Christina Scheidig
Kelvin Y Kwan
Heather G Allore
Richard A Flavell
Albert C Shaw
Office of Infectious Diseases · USYale University · USHarvard University · US

Funding

Yale Study Support Suite (YES3): Dashboard and Web Portal Software Supporting Research Workflow through integrated, customizable REDCap External ModulesP30AG021342 · NIA · YALE UNIVERSITY · PI Denise Esserman · 2002 to 2026
$37.9M
Top3 Homologues in Lymphocyte Genome Stability and AgingR01AG025142 · NIA · YALE UNIVERSITY · PI SHAW, ALBERT C · 2005 to 2009
$1.4M
Blocking TGF-Beta immune signaling as a therapeutic target for Alzheimer's diseasK99AG029726 · NIA · YALE UNIVERSITY · PI TOWN, TERRENCE · 2007 to 2007
$90k
Howard Hughes Medical InstituteNIA NIH HHS 1 K99 AG029726-01NIA NIH HHS K99 AG029726NIA NIH HHS R01 AG025142
6 · The paper itself

Abstract

The type IA topoisomerases have been implicated in the repair of dsDNA breaks by homologous recombination and in the resolution of stalled or damaged DNA replication forks; thus, these proteins play important roles in the maintenance of genomic stability. We studied the functions of one of the two mammalian type IA enzymes, Top3beta, using murine embryonic fibroblasts (MEFs) derived from top3beta(-/-) embryos. top3beta(-/-) MEFs proliferated more slowly than TOP3beta(+/+) control MEFs, demonstrated increased sensitivity to DNA-damaging agents such as ionizing and UV radiation, and had increased DNA double-strand breaks as manifested by increased gamma-H2-AX phosphorylation. However, incomplete enforcement of the G(1)-S cell cycle checkpoint was observed in top3beta(-/-) MEFs. Notably, ataxia-telangiectasia, mutated (ATM)/ATM and Rad3-related (ATR)-dependent substrate phosphorylation after UV-B and ionizing radiation was impaired in top3beta(-/-) versus TOP3beta(+/+) control MEFs, and impaired up-regulation of total and Ser-18-phosphorylated p53 was observed in top3beta(-/-) cells. Taken together, these results suggest an unanticipated role for Top3beta beyond DNA repair in the activation of cellular responses to DNA damage.

Indexed as

DNA DamageAnimalsCell LineCell ProliferationDNA Topoisomerases, Type IHistonesMiceMice, KnockoutMutagensPhosphorylationTumor Suppressor Protein p53DNA Topoisomerases, Type Igamma-H2AX protein, mouseHistonesMutagensTumor Suppressor Protein p53

Identifiers

PMID18367668
PMCPMC2278186
OpenAlexW2098572029

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.