Evidence map›Paper›PMID 21148102›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Rad52 inactivation is synthetically lethal with BRCA2 deficiency.

Zhihui Feng, Shaun P Scott, Wendy Bussen, Girdhar G Sharma, Gongshe Guo, Tej K Pandita, Simon N Powell

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

242 citing papers in PubMed, 339 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Targeting RAD52 overcomes PARP inhibitor resistance in preclinicalbioRxiv : the preprint server for biology · 2025
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Monomers and short oligomers of human RAD52 promote single-strand annealing.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Article
  18. Transcriptomics and Proteomics Analysis of the Liver ofInternational journal of molecular sciences · 2025
    Article
  19. Article
  20. Article

182 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Zhihui FengDepartment of Radiation Oncology, Washington University, St. Louis, MO 63108, USA.
Shaun P Scott
Wendy Bussen
Girdhar G Sharma
Gongshe Guo
Tej K Pandita
Simon N Powell
Washington University in St. Louis · USMemorial Sloan Kettering Cancer Center · US

Funding

Roles of BRCA1, BRCA2 in Homologous RecombinationR01CA107640 · NCI · WASHINGTON UNIVERSITY · PI POWELL, SIMON N. · 2004 to 2008
$1.7M
Functional Characterization of the Mammalian MOF Gene ProductR01CA123232 · NCI · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 2007 to 2011
$1.5M
NCI NIH HHS CA107640NCI NIH HHS CA123232NCI NIH HHS R01 CA107640NCI NIH HHS R01 CA123232
6 · The paper itself

Abstract

Synthetic lethality is a powerful approach to study selective cell killing based on genotype. We show that loss of Rad52 function is synthetically lethal with breast cancer 2, early onset (BRCA2) deficiency, whereas there was no impact on cell growth and viability in BRCA2-complemented cells. The frequency of both spontaneous and double-strand break-induced homologous recombination and ionizing radiation-induced Rad51 foci decreased by 2-10 times when Rad52 was depleted in BRCA2-deficient cells, with little to no effect in BRCA2-complemented cells. The absence of both Rad52 and BRCA2 resulted in extensive chromosome aberrations, especially chromatid-type aberrations. Ionizing radiation-induced and S phase-associated Rad52-Rad51 foci form equally well in the presence or absence of BRCA2, indicating that Rad52 can respond to DNA double-strand breaks and replication stalling independently of BRCA2. Rad52 thus is an independent and alternative repair pathway of homologous recombination and a target for therapy in BRCA2-deficient cells.

Indexed as

Gene Expression Regulation, NeoplasticBRCA2 ProteinCell Line, TumorCell NucleusChromosomal InstabilityChromosome AberrationsDNA DamageGenetic Complementation TestHeLa CellsHumansMicroscopy, FluorescenceRad51 RecombinaseRad52 DNA Repair and Recombination ProteinTetrazolium SaltsThiazolesBRCA2 ProteinBRCA2 protein, humanRAD51 protein, humanRad51 RecombinaseRad52 DNA Repair and Recombination ProteinRAD52 protein, humanTetrazolium SaltsThiazolesthiazolyl blue

Identifiers

PMID21148102
PMCPMC3021033
OpenAlexW2014091491

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.