Evidence map›Paper›PMID 23935957›Full record

ArticlePloS one2013

Nbn and atm cooperate in a tissue and developmental stage-specific manner to prevent double strand breaks and apoptosis in developing brain and eye.

Paulo M G Rodrigues, Paulius Grigaravicius, Martina Remus, Gabriel R Cavalheiro, Anielle L Gomes, Maurício Rocha-Martins, Mauricio R Martins, Lucien Frappart, David Reuss, Peter J McKinnon and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. RINT1 Loss Impairs Retinogenesis Through TRP53-Mediated Apoptosis.Frontiers in cell and developmental biology · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
4 · The record

Corrections and comments

  • Erratum issued
    Martins, Mauricio R [corrected to Rocha-Martins, Maurício]
5 · Who and what money

Authors and funding

13 authors at 5 institutions in 3 countries.

Paulo M G RodriguesPrograma de Biologia Celular e do Desenvolvimento, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Paulius Grigaravicius
Martina Remus
Gabriel R Cavalheiro
Anielle L Gomes
Maurício Rocha-Martins
Mauricio R Martins
Lucien Frappart
David Reuss
Peter J McKinnon
Andreas von Deimling
Rodrigo A P Martins
Pierre-Olivier Frappart
Universidade Federal do Rio de Janeiro · BRHeidelberg University · DEGerman Cancer Research Center · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DESt. Jude Children's Research Hospital · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
The DNA Damage Response and Tumorigenesis in the BrainP01CA096832 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI BAKER, SUZANNE J. · 2003 to 2025
$38.0M
ATM and DNA Damage in the Nervous SystemR01NS037956 · NINDS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI MCKINNON, PETER J · 1998 to 2022
$7.6M
NCI NIH HHS P01 CA096832NCI NIH HHS P30 CA021765NINDS NIH HHS R01 NS037956
6 · The paper itself

Abstract

Nibrin (NBN or NBS1) and ATM are key factors for DNA Double Strand Break (DSB) signaling and repair. Mutations in NBN or ATM result in Nijmegen Breakage Syndrome and Ataxia telangiectasia. These syndromes share common features such as radiosensitivity, neurological developmental defects and cancer predisposition. However, the functional synergy of Nbn and Atm in different tissues and developmental stages is not yet understood. Here, we show in vivo consequences of conditional inactivation of both genes in neural stem/progenitor cells using Nestin-Cre mice. Genetic inactivation of Atm in the central nervous system of Nbn-deficient mice led to reduced life span and increased DSBs, resulting in increased apoptosis during neural development. Surprisingly, the increase of DSBs and apoptosis was found only in few tissues including cerebellum, ganglionic eminences and lens. In sharp contrast, we showed that apoptosis associated with Nbn deletion was prevented by simultaneous inactivation of Atm in developing retina. Therefore, we propose that Nbn and Atm collaborate to prevent DSB accumulation and apoptosis during development in a tissue- and developmental stage-specific manner.

Indexed as

DNA Breaks, Double-StrandedAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsBrainCell Cycle ProteinsCell DifferentiationCerebellumDNA-Binding ProteinsEpistasis, GeneticEyeHomeostasisMiceMice, TransgenicNeural Stem CellsNeuronsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA-Binding ProteinsNijmegen breakage syndrome 1 protein, mouseNuclear Proteins

Identifiers

PMID23935957
PMCPMC3728324
OpenAlexW1964011451

What OpenQuestion holds

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LicenceCC BY
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.