Evidence map›Paper›PMID 21730139›Full record

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

Interhomolog recombination and loss of heterozygosity in wild-type and Bloom syndrome helicase (BLM)-deficient mammalian cells.

Jeannine R LaRocque, Jeremy M Stark, Jin Oh, Ekaterina Bojilova, Kosuke Yusa, Kyoji Horie, Junji Takeda, Maria Jasin

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 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

52 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
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  8. Mechanistic origins of diverse genome rearrangements in cancer.Seminars in cell & developmental biology · 2022
    Review
  9. Article
  10. Review
  11. Article
  12. The Role ofGenes · 2021
    Article
  13. Article
  14. Article
  15. Single-Strand Annealing in Cancer.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Review
  18. Article
  19. POLQ suppresses interhomolog recombination and loss of heterozygosity at targeted DNA breaks.Proceedings of the National Academy of Sciences of the United States of America · 2020
    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 3 institutions in 2 countries.

Jeannine R LaRocqueDevelopmental Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
Jeremy M Stark
Jin Oh
Ekaterina Bojilova
Kosuke Yusa
Kyoji Horie
Junji Takeda
Maria Jasin
Memorial Sloan Kettering Cancer Center · USOsaka University · JPCornell University · US

Funding

RADIATION RESISTANT AND SENSITIVE CELLS DNA BREAK REPAIRR01GM054668 · NIGMS · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI JASIN, MARIA · 1998 to 2015
$5.3M
Gene conversion and end processing mechanisms during double-strand break repairF32GM084637 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI LAROCQUE KAPPAS, JEANNINE · 2008 to 2010
$143k
NIGMS NIH HHS F32 GM084637NIGMS NIH HHS F32GM084637NIGMS NIH HHS R01 GM054668NIGMS NIH HHS R01 GM54668
6 · The paper itself

Abstract

Genomic integrity often is compromised in tumor cells, as illustrated by genetic alterations leading to loss of heterozygosity (LOH). One mechanism of LOH is mitotic crossover recombination between homologous chromosomes, potentially initiated by a double-strand break (DSB). To examine LOH associated with DSB-induced interhomolog recombination, we analyzed recombination events using a reporter in mouse embryonic stem cells derived from F1 hybrid embryos. In this study, we were able to identify LOH events although they occur only rarely in wild-type cells (≤2.5%). The low frequency of LOH during interhomolog recombination suggests that crossing over is rare in wild-type cells. Candidate factors that may suppress crossovers include the RecQ helicase deficient in Bloom syndrome cells (BLM), which is part of a complex that dissolves recombination intermediates. We analyzed interhomolog recombination in BLM-deficient cells and found that, although interhomolog recombination is slightly decreased in the absence of BLM, LOH is increased by fivefold or more, implying significantly increased interhomolog crossing over. These events frequently are associated with a second homologous recombination event, which may be related to the mitotic bivalent structure and/or the cell-cycle stage at which the initiating DSB occurs.

Indexed as

DNA Breaks, Double-StrandedAnimalsBase SequenceBlotting, WesternCell LineChromosomes, MammalianCrossing Over, GeneticCytogenetic AnalysisDNA PrimersElectroporationGene ConversionGenetic VectorsLoss of HeterozygosityMiceMice, Inbred BALB CMolecular Sequence DataBloom syndrome proteinDNA PrimersRecQ Helicases

Identifiers

PMID21730139
PMCPMC3141969
OpenAlexW1963846458

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.