Evidence map›Paper›PMID 19553677›Full record

ArticleThe Journal of biological chemistry2009

MRG15 is a novel PALB2-interacting factor involved in homologous recombination.

Shirley M-H Sy, Michael S Y Huen, Junjie Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

51 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
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  11. Functional Characterization ofFrontiers in molecular biosciences · 2020
    Review
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  17. The Role of PALB2 in the DNA Damage Response and Cancer Predisposition.International journal of molecular sciences · 2017
    Review
  18. MRG15-mediated tethering of PALB2 to unperturbed chromatin protects active genes from genotoxic stress.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
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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

3 authors at 2 institutions in 1 country.

Shirley M-H SyDepartment of Therapeutic Radiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Michael S Y Huen
Junjie Chen
Yale University · USRadiation Oncology Associates · US

Funding

Analysis of BRCA1 Function in DNA RepairR01CA089239 · NCI · YALE UNIVERSITY · PI CHEN, JUNJIE · 2001 to 2015
$3.7M
Study the Role of DNA Damage Responses in Tumorigenesis and SenescenceR01CA092312 · NCI · YALE UNIVERSITY · PI CHEN, JUNJIE · 2001 to 2015
$3.5M
Analysis of 53BP1 function in DNA Damage-signaled pathway and TumorigenesisR01CA100109 · NCI · YALE UNIVERSITY · PI CHEN, JUNJIE · 2003 to 2010
$2.4M
NCI NIH HHS CA089239NCI NIH HHS CA092312NCI NIH HHS CA100109NCI NIH HHS R01 CA089239NCI NIH HHS R01 CA092312NCI NIH HHS R01 CA100109
6 · The paper itself

Abstract

PALB2 is an integral component of the BRCA complex important for recombinational DNA repair. However, exactly how this activity is regulated in vivo remains unexplored. Here we provide evidence to show that MRG15 is a novel PALB2-associated protein that ensures regulated recombination events. We found that the direct interaction between MRG15 and PALB2 is mediated by an evolutionarily conserved region on PALB2. Intriguingly, although damage-induced RAD51 foci formation and mitomycin C sensitivity appeared normal in MRG15-binding defective PALB2 mutants, these cells exhibited a significant increase in gene conversion rates. Consistently, we found that abrogation of the PALB2-MRG15 interaction resulted in elevated sister chromatid exchange frequencies. Our results suggest that loss of the PALB2-MRG15 interaction relieved the cells with the suppression of sister chromatid exchange and therefore led to a hyper-recombination phenotype in the gene conversion assay. Together, our study indicated that although PALB2 is required for proficient homologous recombination, it could also govern the choice of templates used in homologous recombination repair.

Indexed as

Recombination, GeneticCell Line, TumorDNA DamageDNA RepairDose-Response Relationship, DrugFanconi Anemia Complementation Group N ProteinGene DeletionHeLa CellsHumansMitomycinModels, GeneticNuclear ProteinsProtein BindingProtein Structure, TertiarySister Chromatid ExchangeTranscription FactorsFanconi Anemia Complementation Group N ProteinMitomycinMORF4L1 protein, humanNuclear ProteinsPALB2 protein, humanTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID19553677
PMCPMC2755835
OpenAlexW2030351219

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.