ArticleThe Journal of experimental medicine2012
UNG shapes the specificity of AID-induced somatic hypermutation.
Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 49 citations in OpenAlex.
- UNG-RPA interaction governs the choice between high-fidelity and mutagenic uracil repair.Nucleic acids research · 2026Article
- Vaccines combining slow release and follicle targeting of antigens increase germinal center B cell diversity and clonal expansion.Science translational medicine · 2025Article
- Recreation of an antigen-driven germinal center in vitro by providing B cells with phagocytic antigen.Communications biology · 2023Article
- Article
- Deep learning model of somatic hypermutation reveals importance of sequence context beyond hotspot targeting.iScience · 2022Article
- Article
- The role of HIRA-dependent H3.3 deposition and its modifications in the somatic hypermutation of immunoglobulin variable regions.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Tandem Substitutions in Somatic Hypermutation.Frontiers in immunology · 2021Article
- Interplay between UNG and AID governs intratumoral heterogeneity in mature B cell lymphoma.PLoS genetics · 2020Article
- Genetics and epigenetics of leukemia and lymphoma: from knowledge to applications, meeting report of the Josep Carreras Leukaemia Research Institute.Hematological oncology · 2020Review
- Frequent mutations in the amino-terminal domain of BCL7A impair its tumor suppressor role in DLBCL.Leukemia · 2020Article
- Impact of HIV-1 Vpr manipulation of the DNA repair enzyme UNG2 on B lymphocyte class switch recombination.Journal of translational medicine · 2020Article
- Article
- Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID.Nature communications · 2019Article
- Long-read assembly of the Chinese rhesus macaque genome and identification of ape-specific structural variants.Nature communications · 2019Article
- SAMHD1 enhances immunoglobulin hypermutation by promoting transversion mutation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- A broad atlas of somatic hypermutation allows prediction of activation-induced deaminase targets.The Journal of experimental medicine · 2018Article
- Proximity to AGCT sequences dictates MMR-independent versus MMR-dependent mechanisms for AID-induced mutation via UNG2.Nucleic acids research · 2017Article
- CCCTC-Binding Factor Locks Premature IgH Germline Transcription and Restrains Class Switch Recombination.Frontiers in immunology · 2017Article
- Interplay between Target Sequences and Repair Pathways Determines Distinct Outcomes of AID-Initiated Lesions.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Secondary diversification of antibodies through somatic hypermutation (SHM) and class switch recombination (CSR) is a critical component of the immune response. Activation-induced deaminase (AID) initiates both processes by deaminating cytosine residues in immunoglobulin genes. The resulting U:G mismatch can be processed by alternative pathways to give rise to a mutation (SHM) or a DNA double-strand break (CSR). Central to this processing is the activity of uracil-N-glycosylase (UNG), an enzyme normally involved in error-free base excision repair. We used next generation sequencing to analyze the contribution of UNG to the resolution of AID-induced lesions. Loss- and gain-of-function experiments showed that UNG activity can promote both error-prone and high fidelity repair of U:G lesions. Unexpectedly, the balance between these alternative outcomes was influenced by the sequence context of the deaminated cytosine, with individual hotspots exhibiting higher susceptibility to UNG-triggered error-free or error-prone resolution. These results reveal UNG as a new molecular layer that shapes the specificity of AID-induced mutations and may provide new insights into the role of AID in cancer development.
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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.