Evidence map›Paper›PMID 23470994›Full record

ArticleNucleic acids research2013

Concurrent V(D)J recombination and DNA end instability increase interchromosomal trans-rearrangements in ATM-deficient thymocytes.

Steven Bowen, Darawalee Wangsa, Thomas Ried, Ferenc Livak, Richard J Hodes

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Illegitimate recombination between T cell receptor genes in humans and pigs (Sus scrofa domestica).Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2014
    Article
  10. Article
  11. Peripheral subnuclear positioning suppresses Tcrb recombination and segregates Tcrb alleles from RAG2.Proceedings of the National Academy of Sciences of the United States of America · 2013
    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

5 authors at 3 institutions in 1 country.

Steven BowenDepartment of Microbiology and Immunology, Graduate Program in Life Sciences, University of Maryland Baltimore, Baltimore, MD 21201, USA. bowense@mail.nih.gov
Darawalee Wangsa
Thomas Ried
Ferenc Livak
Richard J Hodes
University of Baltimore · USUniversity of Maryland, Baltimore · USNational Cancer Institute · US

Funding

Identification and functional characterization of colorectal cancer genesZIABC010833 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RIED, THOMAS · 2009 to 2022
$12.1M
Analysis of the T Cell RepertoireZIABC009265 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HODES, RICHARD J. · 2009 to 2023
$10.2M
Intramural NIH HHS
6 · The paper itself

Abstract

During the CD4(-)CD8(-) (DN) stage of T-cell development, RAG-dependent DNA breaks and V(D)J recombination occur at three T-cell receptor (TCR) loci: TCRβ, TCRγ and TCRδ. During this stage, abnormal trans-rearrangements also take place between TCR loci, occurring at increased frequency in absence of the DNA damage response mediator ataxia telangiectasia mutated (ATM). Here, we use this model of physiologic trans-rearrangement to study factors that predispose to rearrangement and the role of ATM in preventing chromosomal translocations. The frequency of DN thymocytes with DNA damage foci at multiple TCR loci simultaneously is increased 2- to 3-fold in the absence of ATM. However, trans-rearrangement is increased 10 000- to 100 000-fold, indicating that ATM function extends beyond timely resolution of DNA breaks. RAG-mediated synaptic complex formation occurs between recombination signal sequences with unequal 12 and 23 base spacer sequences (12/23 rule). TCR trans-rearrangements violate this rule, as we observed similar frequencies of 12/23 and aberrant 12/12 or 23/23 recombination products. This suggests that trans-rearrangements are not the result of trans-synaptic complex formation, but they are instead because of unstable cis synaptic complexes that form simultaneously at distinct TCR loci. Thus, ATM suppresses trans-rearrangement primarily through stabilization of DNA breaks at TCR loci.

Indexed as

Gene Rearrangement, T-LymphocyteV(D)J RecombinationAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNADNA-Binding ProteinsDNA BreaksMiceMice, KnockoutProtein Serine-Threonine KinasesThymocytesT-LymphocytesTumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCell Cycle ProteinsDNADNA-Binding ProteinsProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID23470994
PMCPMC3632137
OpenAlexW2009436323

What OpenQuestion holds

Textmetadata
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.