Evidence map›Paper›PMID 14749735›Full record

ArticleThe EMBO journal2004

XRCC3 deficiency results in a defect in recombination and increased endoreduplication in human cells.

Takashi Yoshihara, Mari Ishida, Aiko Kinomura, Mari Katsura, Takanori Tsuruga, Satoshi Tashiro, Toshimasa Asahara, Kiyoshi Miyagawa

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. XRCC3 polymorphism is associated with hypertension-induced left ventricular hypertrophy.Hypertension research : official journal of the Japanese Society of Hypertension · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Polymorphisms in DNA repair genes in gastrointestinal stromal tumours: susceptibility and correlation with tumour characteristics and clinical outcome.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  15. Article
  16. Review
  17. Article
  18. Quality control of homologous recombination.Cellular and molecular life sciences : CMLS · 2014
    Review
  19. Article
  20. 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 1 institution in 1 country.

Takashi YoshiharaDepartment of Human Genetics, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Mari Ishida
Aiko Kinomura
Mari Katsura
Takanori Tsuruga
Satoshi Tashiro
Toshimasa Asahara
Kiyoshi Miyagawa
Hiroshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

XRCC3 was inactivated in human cells by gene targeting. Consistent with its role in homologous recombination, XRCC3(-/-) cells showed a two-fold sensitivity to DNA cross-linking agents, a mild reduction in sister chromatid exchange, impaired Rad51 focus formation and elevated chromosome aberrations. Furthermore, endoreduplication was increased five- seven-fold in the mutants. The T241M variant of XRCC3 has been associated with an increased cancer risk. Expression of the wild-type cDNA restored this phenotype, while expression of the variant restored the defective recombinational repair, but not the increased endoreduplication. RPA, a protein essential for homologous recombination and DNA replication, is associated with XRCC3 and Rad52. Overexpression of RPA promoted endoreduplication, which was partially complemented by overexpression of the wild-type XRCC3 protein, but not by overexpression of the variant protein. Overexpression of Rad52 prevented endoreduplication in RPA-overexpressing cells, in XRCC3(-/-) cells and in the variant-expressing cells, suggesting that deregulated RPA was responsible for the increased endoreduplication. These observations offer the first genetic evidence for the association between homologous recombination and replication initiation having a role in cancer susceptibility.

Indexed as

PloidiesRecombination, GeneticAgmatineCell LineChromosomes, HumanCross-Linking ReagentsDNA-Binding ProteinsDNA, ComplementaryDNA DamageDNA RepairGene DeletionGene ExpressionGene TargetingHumansMitomycinRad52 DNA Repair and Recombination ProteinAgmatineCross-Linking ReagentsDNA-Binding ProteinsDNA, ComplementaryMitomycinMMC complexRad52 DNA Repair and Recombination ProteinRAD52 protein, humanReplication Protein ARPA1 protein, humanSuccinatesX-ray repair cross complementing protein 3

Identifiers

PMID14749735
PMCPMC1271813
OpenAlexW2129499391

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.