Evidence map›Paper›PMID 12509447›Full record

ArticleMolecular and cellular biology2003

Enhanced genomic instability and defective postreplication repair in RAD18 knockout mouse embryonic stem cells.

Satoshi Tateishi, Hitoshi Niwa, Jun-Ichi Miyazaki, Shiho Fujimoto, Hirokazu Inoue, Masaru Yamaizumi

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

68 citing papers in PubMed, 118 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Impacts of arsenic on Rad18 and translesion synthesis.Toxicology and applied pharmacology · 2022
    Article
  9. Article
  10. DNA repair fidelity in stem cell maintenance, health, and disease.Biochimica et biophysica acta. Molecular basis of disease · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. [Effect of RAD18-siRNA on proliferation and chemotherapy sensitivity of human esophageal squamous cell carcinoma ECA-109 cells].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2016
    Article
  17. Article
  18. Article
  19. Article
  20. Tumor suppressor miR-145 reverses drug resistance by directly targeting DNA damage-related gene RAD18 in colorectal cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article

8 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

6 authors at 3 institutions in 1 country.

Satoshi TateishiInstitute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 862-0976, USA.
Hitoshi Niwa
Jun-Ichi Miyazaki
Shiho Fujimoto
Hirokazu Inoue
Masaru Yamaizumi
Kumamoto University · JPOsaka University · JPSaitama University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In lower eukaryotes, Rad18 plays a crucial role in postreplication repair. Previously, we isolated a human homologue of RAD18 (hRAD18) and showed that human cells overexpressing hRad18 protein with a mutation in the RING finger motif are defective in postreplication repair. Here, we report the construction of RAD18-knockout mouse embryonic stem cells by gene targeting. These cells had almost the same growth rate as wild-type cells and manifested phenotypes similar to those of human cells expressing mutant Rad18 protein: hypersensitivity to multiple DNA damaging agents and a defect in postreplication repair. Mutation was not induced in the knockout cells with any higher frequencies than in wild-type cells, as shown by ouabain resistance. In the knockout cells, spontaneous sister chromatid exchange (SCE) occurred with twice the frequency observed in normal cells. After mild DNA damage, SCE was threefold higher in the knockout cells, while no increase was observed in normal cells. Stable transformation efficiencies were approximately 20-fold higher in knockout cells, and gene targeting occurred with approximately 40-fold-higher frequency than in wild-type cells at the Oct3/4 locus. These results indicate that dysfunction of Rad18 greatly increases both the frequency of homologous as well as illegitimate recombination, and that RAD18 contributes to maintenance of genomic stability through postreplication repair.

Indexed as

DNA RepairSaccharomyces cerevisiae ProteinsAmino Acid MotifsAnimalsCOS CellsDNADNA-Binding ProteinsDNA, ComplementaryDNA DamageDose-Response Relationship, DrugGlutathione TransferaseHumansImmunohistochemistryLigasesMiceMice, KnockoutDNADNA-Binding ProteinsDNA, ComplementaryGlutathione TransferaseLigasesMutagensRAD18 protein, humanRAD18 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsUbiquitin-Conjugating EnzymesUbiquitin-Protein Ligases

Identifiers

PMID12509447
PMCPMC151530
OpenAlexW2100771513

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.