ArticleProceedings of the National Academy of Sciences of the United States of America2001
Intermediates in V(D)J recombination: a stable RAG1/2 complex sequesters cleaved RSS ends.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
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Who cites it
41 citing papers in PubMed, 79 citations in OpenAlex.
- Temporally uncoupled signal and coding joint formation in human V(D)J recombination.Molecular immunology · 2020Article
- The ATM Kinase Restrains Joining of Both VDJ Signal and Coding Ends.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Restoration of ATM Expression in DNA-PKcs-Deficient Cells Inhibits Signal End Joining.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Assembly Pathway and Characterization of the RAG1/2-DNA Paired and Signal-end Complexes.The Journal of biological chemistry · 2015Article
- Article
- A hypomorphic recombination-activating gene 1 (RAG1) mutation resulting in a phenotype resembling common variable immunodeficiency.The Journal of allergy and clinical immunology · 2014Article
- Modeling of the RAG reaction mechanism.Cell reports · 2014Article
- Functional overlaps between XLF and the ATM-dependent DNA double strand break response.DNA repair · 2014Review
- RAG2's acidic hinge restricts repair-pathway choice and promotes genomic stability.Cell reports · 2013Article
- Real-time monitoring of RAG-catalyzed DNA cleavage unveils dynamic changes in coding end association with the coding end complex.Nucleic acids research · 2012Article
- XRCC4's interaction with XLF is required for coding (but not signal) end joining.Nucleic acids research · 2012Article
- The response to and repair of RAG-mediated DNA double-strand breaks.Annual review of immunology · 2012Review
- Lymphocyte development: integration of DNA damage response signaling.Advances in immunology · 2012Review
- Repair of chromosomal RAG-mediated DNA breaks by mutant RAG proteins lacking phosphatidylinositol 3-like kinase consensus phosphorylation sites.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Unique and redundant functions of ATM and DNA-PKcs during V(D)J recombination.Cell cycle (Georgetown, Tex.) · 2011Review
- 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 · 2011Article
- Non-consensus heptamer sequences destabilize the RAG post-cleavage complex, making ends available to alternative DNA repair pathways.Nucleic acids research · 2010Article
- Replication independent DNA double-strand break retention may prevent genomic instability.Molecular cancer · 2010Article
- Cytosines, but not purines, determine recombination activating gene (RAG)-induced breaks on heteroduplex DNA structures: implications for genomic instability.The Journal of biological chemistry · 2010Article
- Requirement for ubiquitin conjugation and 26S proteasome activity at an early stage in V(D)J recombination.Molecular immunology · 2010Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Rearrangement of gene segments to generate antigen receptor coding regions depends on the RAG1/2 recombinase, which assembles a synaptic complex between two DNA signal sequences and then cleaves the DNA directly adjacent to the paired signals. After coupled cleavage of complementary signal sequences, virtually all of the cleaved signal ends remained associated with RAG1/2 in stable complexes. These signal end complexes were distinct from various precleavage RAG1/2 signal complexes in that they were resistant to treatment with heparin. A mammalian joining apparatus consisting of purified Ku70/86, XRCC4, and DNA ligase IV proteins was sufficient to join deproteinized cleaved ends, but retention of signal sequences within the signal end complex blocked access to the DNA ends and prevented their joining by these proteins. Sequestration of cleaved ends within the signal end complex would account for the persistence of these ends in the cell after cleavage and may explain why they do not normally activate the DNA-damage-dependent cell cycle checkpoint.
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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.