Evidence map›Paper›PMID 20446816›Full record

ArticleStem cells and development2010

Mouse embryonic stem cells, but not somatic cells, predominantly use homologous recombination to repair double-strand DNA breaks.

Elisia D Tichy, Resmi Pillai, Li Deng, Li Liang, Jay Tischfield, Sandy J Schwemberger, George F Babcock, Peter J Stambrook

Open access · greenAbstract read
In one paragraph

Article in Stem cells and development, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing 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

98 citing papers in PubMed, 150 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Embryonic Stem Cell-Specific Responses to DNA Replication Stress.bioRxiv : the preprint server for biology · 2025
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. DPPA5A suppresses the mutagenic TLS and MMEJ pathways by modulating the cryptic splicing ofProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  15. Article
  16. Science advances · 2023
    Article
  17. Science advances · 2023
    Article
  18. Article
  19. Article
  20. Article

38 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

8 authors at 4 institutions in 1 country.

Elisia D TichyDepartment of Cell and Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0524, USA. tichyed@ucmail.uc.edu
Resmi Pillai
Li Deng
Li Liang
Jay Tischfield
Sandy J Schwemberger
George F Babcock
Peter J Stambrook
Rutgers, The State University of New Jersey · USShriners Hospitals for Children - Erie · USUniversity of Cincinnati Medical Center · USUniversity of Cincinnati · US

Funding

ENVIRONMETAL CARCINOGENESIS AND MUTAGENESIST32ES007250 · NIEHS · UNIVERSITY OF CINCINNATI · PI MILLER, WILLIAM E · 1988 to 2024
$11.9M
Pathways to Mutagenesis in vivo and in Stem CellsR01ES012695 · NIEHS · UNIVERSITY OF CINCINNATI · PI STAMBROOK, PETER J. · 2006 to 2009
$1.7M
NIEHS NIH HHS R01 ES012695NIEHS NIH HHS R01 ES12695-4S1NIEHS NIH HHS T32 ES007250-21
6 · The paper itself

Abstract

Embryonic stem (ES) cells give rise to all cell types of an organism. Since mutations at this embryonic stage would affect all cells and be detrimental to the overall health of an organism, robust mechanisms must exist to ensure that genomic integrity is maintained. To test this proposition, we compared the capacity of murine ES cells to repair DNA double-strand breaks with that of differentiated cells. Of the 2 major pathways that repair double-strand breaks, error-prone nonhomologous end joining (NHEJ) predominated in mouse embryonic fibroblasts, whereas the high fidelity homologous recombinational repair (HRR) predominated in ES cells. Microhomology-mediated end joining, an emerging repair pathway, persisted at low levels in all cell types examined. The levels of proteins involved in HRR and microhomology-mediated end joining were highly elevated in ES cells compared with mouse embryonic fibroblasts, whereas those for NHEJ were quite variable, with DNA Ligase IV expression low in ES cells. The half-life of DNA Ligase IV protein was also low in ES cells. Attempts to increase the abundance of DNA Ligase IV protein by overexpression or inhibition of its degradation, and thereby elevate NHEJ in ES cells, were unsuccessful. When ES cells were induced to differentiate, however, the level of DNA Ligase IV protein increased, as did the capacity to repair by NHEJ. The data suggest that preferential use of HRR rather than NHEJ may lend ES cells an additional layer of genomic protection and that the limited levels of DNA Ligase IV may account for the low level of NHEJ activity.

Indexed as

DNA Breaks, Double-StrandedDNA RepairRecombination, GeneticAnimalsAntineoplastic AgentsCells, CulturedDNA Ligase ATPDNA LigasesEmbryonic Stem CellsFibroblastsMiceMice, Inbred C57BLTretinoinAntineoplastic AgentsDNA Ligase ATPDNA LigasesTretinoin

Identifiers

PMID20446816
PMCPMC3128311
OpenAlexW2033411843

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.