ReviewOncogene2007
Breaking down cell cycle checkpoints and DNA repair during antigen receptor gene assembly.
Review in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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.
Who cites it
17 citing papers in PubMed.
- Review
- POLE2 knockdown suppresses lymphoma progression via downregulating Wnt/β-catenin signaling pathway.Molecular and cellular biochemistry · 2024Article
- A novel mutation in the POLE2 gene causing combined immunodeficiency.The Journal of allergy and clinical immunology · 2016Article
- CHK2 kinase in the DNA damage response and beyond.Journal of molecular cell biology · 2014Review
- Checkpoint kinase 1 negatively regulates somatic hypermutation.Nucleic acids research · 2014Article
- 53BP1 mediates productive and mutagenic DNA repair through distinct phosphoprotein interactions.Cell · 2013Article
- The RAG2 C-terminus and ATM protect genome integrity by controlling antigen receptor gene cleavage.Nature communications · 2013Article
- Article
- Close proximity to Igh is a contributing factor to AID-mediated translocations.Molecular cell · 2012Article
- Mass spectrometry analysis and quantitation of peptides presented on the MHC II molecules of mouse spleen dendritic cells.Journal of proteome research · 2011Article
- ATMIN is required for maintenance of genomic stability and suppression of B cell lymphoma.Cancer cell · 2011Article
- Critical requirement of GABPalpha for normal T cell development.The Journal of biological chemistry · 2010Article
- Epigenetic regulation of antigen receptor gene rearrangement.F1000 biology reports · 2010Article
- From pathogenesis to treatment of chronic lymphocytic leukaemia.Nature reviews. Cancer · 2010Review
- Deficiency of the DNA repair enzyme ATM in rheumatoid arthritis.The Journal of experimental medicine · 2009Article
- The ageing immune system: is it ever too old to become young again?Nature reviews. Immunology · 2009Review
- Multiple autophosphorylation sites are dispensable for murine ATM activation in vivo.The Journal of cell biology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Double-strand breaks (DSBs) are intermediates in several physiological processes including V(D)J and class switch recombination. They are also potent substrates for chromosomal translocations that arise as by-products of antigen receptor gene assembly in lymphocytes. ATM is one among several key proteins involved in the detection, signaling and repair of DNA breaks. Despite redundancies in DSB signaling pathways, it has recently been demonstrated that ATM deficient lymphocytes can survive and proliferate several generations in vitro and in vivo despite harboring terminally deleted chromosomes produced by V(D)J recombination. In this review, we discuss how two complementary genome maintenance functions mediated by ATM prevent lymphocytes from adapting to persistent DNA damage.
Indexed as
Identifiers
18066088What OpenQuestion holds
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.