ArticleMolecular and cellular biology2002
Targeted transposition by the V(D)J recombinase.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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.
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Who cites it
25 citing papers in PubMed, 51 citations in OpenAlex.
- Recombination between fragile regions associated with chromosomal rearrangements in glioblastoma can be mediated by RAGs.iScience · 2025Article
- Different classes of genomic inserts contribute to human antibody diversity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- RAG1/2 induces genomic insertions by mobilizing DNA into RAG1/2-independent breaks.The Journal of experimental medicine · 2017Article
- Role of recombination activating genes in the generation of antigen receptor diversity and beyond.Immunology · 2012Review
- The distribution of inverted repeat sequences in the Saccharomyces cerevisiae genome.Current genetics · 2010Article
- V(D)J recombination: Born to be wild.Seminars in cancer biology · 2010Review
- Genome-wide analysis of Tol2 transposon reintegration in zebrafish.BMC genomics · 2009Article
- Chromosome 12p deletions in TEL-AML1 childhood acute lymphoblastic leukemia are associated with retrotransposon elements and occur postnatally.Cancer research · 2008Article
- Understanding how the V(D)J recombinase catalyzes transesterification: distinctions between DNA cleavage and transposition.Nucleic acids research · 2008Article
- Article
- In vivo reinsertion of excised episomes by the V(D)J recombinase: a potential threat to genomic stability.PLoS biology · 2007Article
- Target DNA structure plays a critical role in RAG transposition.PLoS biology · 2006Article
- Genomic instability due to V(D)J recombination-associated transposition.Genes & development · 2006Article
- Monitoring single-stranded DNA secondary structure formation by determining the topological state of DNA catenanes.Biophysical journal · 2006Article
- Double-strand break formation by the RAG complex at the bcl-2 major breakpoint region and at other non-B DNA structures in vitro.Molecular and cellular biology · 2005Article
- DNA cleavage activity of the V(D)J recombination protein RAG1 is autoregulated.Molecular and cellular biology · 2004Article
- In vitro processing of the 3'-overhanging DNA in the postcleavage complex involved in V(D)J joining.Molecular and cellular biology · 2004Article
- Ordered DNA release and target capture in RAG transposition.The EMBO journal · 2004Article
- DNA mismatches and GC-rich motifs target transposition by the RAG1/RAG2 transposase.Nucleic acids research · 2003Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cleavage by the V(D)J recombinase at a pair of recombination signal sequences creates two coding ends and two signal ends. The RAG proteins can integrate these signal ends, without sequence specificity, into an unrelated target DNA molecule. Here we demonstrate that such transposition events are greatly stimulated by--and specifically targeted to--hairpins and other distorted DNA structures. The mechanism of target selection by the RAG proteins thus appears to involve recognition of distorted DNA. These data also suggest a novel mechanism for the formation of alternative recombination products termed hybrid joints, in which a signal end is joined to a hairpin coding end. We suggest that hybrid joints may arise by transposition in vivo and propose a new model to account for some recurrent chromosome translocations found in human lymphomas. According to this model, transposition can join antigen receptor loci to partner sites that lack recombination signal sequence elements but bear particular structural features. The RAG proteins are capable of mediating all necessary breakage and joining events on both partner chromosomes; thus, the V(D)J recombinase may be far more culpable for oncogenic translocations than has been suspected.
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Registered trials
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.