Evidence map›Paper›PMID 15064730›Full record

ArticleOncogene2004

The mismatch DNA repair heterodimer, hMSH2/6, regulates BLM helicase.

Qin Yang, Ran Zhang, Xin W Wang, Steven P Linke, Sagar Sengupta, Ian D Hickson, Graziella Pedrazzi, Claudia Perrera, Igor Stagljar, Susan J Littman and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Coordinated roles of SLX4 and MutSβ in DNA repair and the maintenance of genome stability.Critical reviews in biochemistry and molecular biology · 2021
    Review
  14. Article
  15. DNA Mismatch Repair Gene Variants in Sporadic Solid Cancers.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Review
  18. Article
  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

12 authors at 4 institutions in 3 countries.

Qin YangLaboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bldg 37, Rm 3068, 37 Convent Drive, Bethesda, MD 20892-4255, USA.
Ran Zhang
Xin W Wang
Steven P Linke
Sagar Sengupta
Ian D Hickson
Graziella Pedrazzi
Claudia Perrera
Igor Stagljar
Susan J Littman
Paul Modrich
Curtis C Harris
National Cancer Institute · USUniversity of Zurich · CHDuke Medical Center · USCancer Research UK · GB

Funding

Enzymology Of Eukaryotic Mismatch RepairR01GM045190 · NIGMS · DUKE UNIVERSITY · PI MODRICH, PAUL LAWRENCE · 1991 to 2018
$6.8M
p53 Tumor Suppressor PathwayZIABC005795 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 2009 to 2012
$3.0M
p53 Tumor Suppressor PathwayZ01BC005795 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 1996 to 2008
$2.3M
NIGMS NIH HHS GM45190
6 · The paper itself

Abstract

The human MSH2/6 complex is essential for mismatch recognition during the repair of replication errors. Although mismatch repair components have been implicated in DNA homologous recombination repair, the exact function of hMSH2/6 in this pathway is unclear. Here, we show that the recombinant hMSH2/6 protein complex stimulated the ability of the Bloom's syndrome gene product, BLM, to process Holliday junctions in vitro, an activity that could also be regulated by p53. Consistent with these observations, hMSH6 colocalized with BLM and phospho-ser15-p53 in hydroxyurea-induced RAD51 nuclear foci that may correspond to the sites of presumed stalled DNA replication forks and more likely the resultant DNA double-stranded breaks. In addition, we show that hMSH2 and hMSH6 coimmunoprecipitated with BLM, p53, and RAD51. Both the number of RAD51 foci and the amount of the BLM-p53-RAD51 complex are increased in hMSH2- or hMSH6-deficient cells. These data suggest that hMSH2/6 formed a complex with BLM-p53-RAD51 in response to the damaged DNA forks during double-stranded break repair.

Indexed as

DNA RepairAdenosine TriphosphatasesBase Pair MismatchCell Line, TumorDimerizationDNA-Binding ProteinsDNA HelicasesFemaleHumansMutS Homolog 2 ProteinProto-Oncogene ProteinsRad51 RecombinaseRecQ HelicasesTumor Suppressor Protein p53Adenosine TriphosphatasesBloom syndrome proteinDNA-Binding ProteinsDNA HelicasesG-T mismatch-binding proteinMSH2 protein, humanMutS Homolog 2 ProteinProto-Oncogene ProteinsRAD51 protein, humanRad51 RecombinaseRecQ HelicasesTumor Suppressor Protein p53

Identifiers

PMID15064730
OpenAlexW2028785832

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.