Evidence map›Paper›PMID 26338419›Full record

ArticleGenes & development2015

MERIT40 cooperates with BRCA2 to resolve DNA interstrand cross-links.

Qinqin Jiang, Manikandan Paramasivam, Bernadette Aressy, Junmin Wu, Marina Bellani, Wei Tong, Michael M Seidman, Roger A Greenberg

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed, 24 citations in OpenAlex.

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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

8 authors at 4 institutions in 1 country.

Qinqin JiangDepartment of Cancer Biology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA; Department of Pathology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Manikandan ParamasivamLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA;
Bernadette AressyDepartment of Cancer Biology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA; Department of Pathology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Junmin WuDepartment of Cancer Biology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA; Department of Pathology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Marina BellaniLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA;
Wei TongDivision of Hematology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA.
Michael M SeidmanLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA;
Roger A GreenbergDepartment of Cancer Biology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA; Department of Pathology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
National Institutes of Health · USCancer Research Institute · USParker Institute for Cancer Immunotherapy · USChildren's Hospital of Philadelphia · US

Funding

VIRAL VECTOR COREP30DK019525 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI MITCHELL A. LAZAR · 1986 to 2026
$48.3M
Repair of localized DNA damageZIAAG000746 · NIA · NATIONAL INSTITUTE ON AGING · PI SEIDMAN, MICHAEL · 2009 to 2025
$30.0M
Lnk Regulatory Functions in Hematopoietic Stem CellsR01HL095675 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI TONG, WEI · 2009 to 2021
$5.6M
The RAP80-BRCC36 Deubiquitinating Complex in DNA RepairR01CA138835 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Roger A Greenberg · 2010 to 2026
$5.2M
DNA Double Strand Break Chromatin Alterations and Genome IntegrityR01GM101149 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI GREENBERG, ROGER A · 2013 to 2025
$4.0M
Regulation of protein ubiquitination in hematopoietic cytokine signalingR01HL133828 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI TONG, WEI · 2017 to 2020
$2.2M
Repair of localized DNA damageZ01AG000746 · NIA · NATIONAL INSTITUTE ON AGING · PI SEIDMAN, MICHAEL · 2007 to 2008
$607k
Intramural NIH HHS Z01 AG000746NCI NIH HHS CA17494NCI NIH HHS R01 CA138835NHLBI NIH HHS R01 HL095675NHLBI NIH HHS R01 HL133828NIA NIH HHS ZO1 AG000746-08NIDDK NIH HHS P30 DK019525NIGMS NIH HHS GM101149NIGMS NIH HHS R01 GM101149PHS HHS A138835
6 · The paper itself

Abstract

MERIT40 is an essential component of the RAP80 ubiquitin recognition complex that targets BRCA1 to DNA damage sites. Although this complex is required for BRCA1 foci formation, its physiologic role in DNA repair has remained enigmatic, as has its relationship to canonical DNA repair mechanisms. Surprisingly, we found that Merit40(-/-) mice displayed marked hypersensitivity to DNA interstrand cross-links (ICLs) but not whole-body irradiation. MERIT40 was rapidly recruited to ICL lesions prior to FANCD2, and Merit40-null cells exhibited delayed ICL unhooking coupled with reduced end resection and homologous recombination at ICL damage. Interestingly, Merit40 mutation exacerbated ICL-induced chromosome instability in the context of concomitant Brca2 deficiency but not in conjunction with Fancd2 mutation. These findings implicate MERIT40 in the earliest stages of ICL repair and define specific functional interactions between RAP80 complex-dependent ubiquitin recognition and the Fanconi anemia (FA)-BRCA ICL repair network.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBRCA2 ProteinCell Cycle ProteinsCell LineChromosomal InstabilityDNA-Binding ProteinsDNA DamageDNA HelicasesDNA RepairFanconi Anemia Complementation Group D2 ProteinHistone ChaperonesHumansMiceMice, Inbred C57BLMutationAdaptor Proteins, Signal TransducingBRCA2 ProteinBRCA2 protein, mouseCell Cycle ProteinsDNA-Binding ProteinsDNA HelicasesFancd2 protein, mouseFanconi Anemia Complementation Group D2 ProteinHistone ChaperonesMERIT40 protein, mouseRap80 protein, mouseTranscription FactorsBRCA2DNA2interstrand cross-link repairMERIT40ubiquitination

Identifiers

PMID26338419
PMCPMC4579352
OpenAlexW2198913091

What OpenQuestion holds

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LicenceCC BY-NC
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.