Evidence map›Paper›PMID 19362533›Full record

ArticleMolecular cell2009

Roles for NBS1 in alternative nonhomologous end-joining of V(D)J recombination intermediates.

Ludovic Deriano, Travis H Stracker, Annalee Baker, John H J Petrini, David B Roth

Abstract read
In one paragraph

Article in Molecular cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing 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

82 citing papers in PubMed.

  1. Article
  2. Differential expression of a disease-associatedbioRxiv : the preprint server for biology · 2025
    Article
  3. NBS1 facilitates preribosomal RNA biogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Polymerase δ promotes chromosomal rearrangements and imprecise double-strand break repair.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Article
  13. Nbn-Mre11 interaction is required for tumor suppression and genomic integrity.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

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

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

5 authors.

Ludovic DerianoDepartment of Pathology, The Helen L and Martin S. Kimmel Center for Biology and Medicine at the Skirball Institute for Biomolecular Medicine and , New York University School of Medicine, New York, NY 10016, USA.
Travis H Stracker
Annalee Baker
John H J Petrini
David B Roth

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
The Mre11 complex: linking recombination to checkpointsR01GM059413 · NIGMS · UNIVERSITY OF WISCONSIN MADISON · PI PETRINI, JOHN HJ · 1999 to 2011
$5.2M
RAG-induced DNA damage: mechanisms and responsesR01CA104588 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROTH, DAVID B. · 2004 to 2014
$2.8M
V(D)J recombination, genomic instability, and cancerR01CA096764 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ROTH, DAVID B. · 2002 to 2006
$1.9M
FASEB SRC on Genetic Recombination and Genome RearrangementsR13CA162528 · NCI · FEDERATION OF AMER SOC FOR EXPER BIOLOGY · PI PETRINI, JOHN HJ · 2011 to 2011
$5k
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA096764NCI NIH HHS R01 CA104588NCI NIH HHS R13 CA162528NIGMS NIH HHS R01 GM059413
6 · The paper itself

Abstract

Recent work has highlighted the importance of alternative, error-prone mechanisms for joining DNA double-strand breaks (DSBs) in mammalian cells. These noncanonical, nonhomologous end-joining (NHEJ) pathways threaten genomic stability but remain poorly characterized. The RAG postcleavage complex normally prevents V(D)J recombination-associated DSBs from accessing alternative NHEJ. Because the MRE11/RAD50/NBS1 complex localizes to RAG-mediated DSBs and possesses DNA end tethering, processing, and joining activities, we asked whether it plays a role in the mechanism of alternative NHEJ or participates in regulating access of DSBs to alternative repair pathways. We find that NBS1 is required for alternative NHEJ of hairpin coding ends, suppresses alternative NHEJ of signal ends, and promotes proper resolution of inversional recombination intermediates. These data demonstrate that the MRE11 complex functions at two distinct levels, regulating repair pathway choice (likely through enhancing the stability of DNA end complexes) and participating in alternative NHEJ of coding ends.

Indexed as

DNA Breaks, Double-StrandedRecombination, GeneticAcid Anhydride HydrolasesAnimalsATP-Binding Cassette TransportersCell Cycle ProteinsCells, CulturedDNA-Binding ProteinsDNA RepairDNA Repair EnzymesEndonucleasesMiceMRE11 Homologue ProteinMutationNuclear ProteinsProtein Kinase CAcid Anhydride HydrolasesATP-Binding Cassette TransportersCell Cycle ProteinsDclre1c protein, mouseDNA-Binding ProteinsDNA Repair EnzymesEndonucleasesMre11a protein, mouseMRE11 Homologue ProteinNijmegen breakage syndrome 1 protein, mouseNuclear ProteinsProtein Kinase CRad50 protein, mouseVDJ Recombinases

Identifiers

PMID19362533
PMCPMC2704125

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Registered trials

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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.