Evidence map›Paper›PMID 17502661›Full record

ArticleThe Journal of experimental medicine2007

Defects in coding joint formation in vivo in developing ATM-deficient B and T lymphocytes.

Ching-Yu Huang, Girdhar G Sharma, Laura M Walker, Craig H Bassing, Tej K Pandita, Barry P Sleckman

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. The ATM Kinase Restrains Joining of Both VDJ Signal and Coding Ends.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Article
  8. Article
  9. Article
  10. Article
  11. 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
  12. Quality control of homologous recombination.Cellular and molecular life sciences : CMLS · 2014
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Ching-Yu HuangDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Girdhar G Sharma
Laura M Walker
Craig H Bassing
Tej K Pandita
Barry P Sleckman
Washington University in St. Louis · USChildren's Hospital of Philadelphia · US

Funding

THE V(D)J RECOMBINATION REACTION AND ITS IMPACT ON LYMPHOCYTE DEVELOPMENTR01AI047829 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SLECKMAN, BARRY P · 2000 to 2021
$7.0M
CONTROL OF TCR V BETA REARRANGEMENT &ALLELIC EXCLUSIONR01AI049934 · NIAID · DUKE UNIVERSITY · PI KRANGEL, MICHAEL S · 2001 to 2015
$6.8M
CHROMATIN-TELOMERE STRUCTURE AND AT GENOMIC SENSITIVITYR01NS034746 · NINDS · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 1996 to 2005
$1.2M
ANIMAL SPACE FOR CARDIOVASCULAR AND ONCOLOGY RESEARCHC06RR012466 · NCRR · WASHINGTON UNIVERSITY · PI CICERO, THEODORE J · 1997 to 1997
–
NCI NIH HHS CA10445NCRR NIH HHS RR012466NIAID NIH HHS AI47829NIAID NIH HHS AI4993NIAID NIH HHS R01 AI047829NIAID NIH HHS R01 AI049934NINDS NIH HHS NS34746NINDS NIH HHS R01 NS034746
6 · The paper itself

Abstract

Ataxia-telangiectasia mutated (ATM)-deficient lymphocytes exhibit defects in coding joint formation during V(D)J recombination in vitro. Similar defects in vivo should affect both T and B cell development, yet the lymphoid phenotypes of ATM deficiency are more pronounced in the T cell compartment. In this regard, ATM-deficient mice exhibit a preferential T lymphopenia and have an increased incidence of nontransformed and transformed T cells with T cell receptor alpha/delta locus translocations. We demonstrate that there is an increase in the accumulation of unrepaired coding ends during different steps of antigen receptor gene assembly at both the immunoglobulin and T cell receptor loci in developing ATM-deficient B and T lymphocytes. Furthermore, we show that the frequency of ATM-deficient alphabeta T cells with translocations involving the T cell receptor alpha/delta locus is directly related to the number of T cell receptor alpha rearrangements that these cells can make during development. Collectively, these findings demonstrate that ATM deficiency leads to broad defects in coding joint formation in developing B and T lymphocytes in vivo, and they provide a potential molecular explanation as to why the developmental impact of these defects could be more pronounced in the T cell compartment.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsBlotting, SouthernB-LymphocytesCell Cycle ProteinsDNA-Binding ProteinsFlow CytometryImmunoglobulin Joining RegionMicePolymerase Chain ReactionProtein Serine-Threonine KinasesReceptors, Antigen, T-CellRecombination, GeneticT-LymphocytesTumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsImmunoglobulin Joining RegionProtein Serine-Threonine KinasesReceptors, Antigen, T-CellTumor Suppressor Proteins

Identifiers

PMID17502661
PMCPMC2118620
OpenAlexW2051639914

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.