Evidence map›Paper›PMID 16449665›Full record

ArticleMolecular and cellular biology2006

Mobilization of RAG-generated signal ends by transposition and insertion in vivo.

Monalisa Chatterji, Chia-Lun Tsai, David G Schatz

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 54 citations in OpenAlex.

  1. How RAG1/2 evolved from ancestral transposases to initiate V(D)J recombination without transposition.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Detection of chromosomal alteration after infusion of gene-edited allogeneic CAR T cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. How mouse RAG recombinase avoids DNA transposition.Nature structural & molecular biology · 2020
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Ataxia telangiectasia-mutated protein and DNA-dependent protein kinase have complementary V(D)J recombination functions.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  16. Ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases have overlapping activities during chromosomal signal joint formation.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  17. V(D)J recombination: Born to be wild.Seminars in cancer biology · 2010
    Review
  18. Review
  19. RAG: a recombinase diversified.Nature immunology · 2009
    Review
  20. Nuclear localization of p38 MAPK in response to DNA damage.International journal of biological sciences · 2009
    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

3 authors at 1 institution in 1 country.

Monalisa ChatterjiHoward Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, 300 Cedar Street, Box 208011, New Haven, CT 06520-8011, USA.
Chia-Lun Tsai
David G Schatz
Howard Hughes Medical Institute · US

Funding

Mechanism and Targeting of V(D)J RecombinationR01AI032524 · NIAID · YALE UNIVERSITY · PI David G. Schatz · 1992 to 2026
$6.7M
Immunoglobulin and T Cell Receptor Gene AssemblyR37AI032524 · NIAID · YALE UNIVERSITY · PI SCHATZ, DAVID G. · 2007 to 2016
$3.5M
NIAID NIH HHS AI32524NIAID NIH HHS R01 AI032524NIAID NIH HHS R37 AI032524
6 · The paper itself

Abstract

In addition to their essential roles in V(D)J recombination, the RAG proteins have been found to catalyze transposition in vitro, but it has been difficult to demonstrate transposition by the RAG proteins in vivo in vertebrate cells. As genomic instability and chromosomal translocations are common outcomes of transposition in other species, it is critical to understand if the RAG proteins behave as a transposase in vertebrate cells. To facilitate this, we have developed an episome-based assay to detect products of RAG-mediated transposition in the human embryonic kidney cell line 293T. Transposition events into the target episome, accompanied by characteristic target site duplications, were detected at a low frequency using RAG1 and either truncated "core" RAG2 or full-length RAG2. More frequently, insertion of the RAG-generated signal end fragment into the target was accompanied by deletions or more complex rearrangements, and our data indicate that these events occur by a mechanism that is distinct from transposition. An assay to detect transposition from an episome into the human genome failed to detect bona fide transposition events but instead yielded chromosome deletion and translocation events involving the signal end fragment mobilized by the RAG proteins. These assays provide a means of assessing RAG-mediated transposition in vivo, and our findings provide insight into the potential for the products of RAG-mediated DNA cleavage to cause genome instability.

Indexed as

Base SequenceCell LineDNADNA-Binding ProteinsHomeodomain ProteinsHumansNuclear ProteinsPlasmidsProtein Sorting SignalsRecombinant ProteinsSequence DeletionTransposasesDNADNA-Binding ProteinsHomeodomain ProteinsNuclear ProteinsProtein Sorting SignalsRAG-1 proteinRAG2 protein, humanRecombinant ProteinsTransposases

Identifiers

PMID16449665
PMCPMC1367191
OpenAlexW2107769824

What OpenQuestion holds

Textmetadata
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.