ArticleThe Journal of experimental medicine2016
UNG protects B cells from AID-induced telomere loss.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05025098 (Precision Therapy Versus Standard Therapy in Acute Myeloid Leukaemia and Myelodysplastic Syndrome in Elderly), which is not on this map. Cited by 20 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.
Precision Therapy Versus Standard Therapy in Acute Myeloid Leukaemia and Myelodysplastic Syndrome in Elderly
Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Multivariable genome-wide analysis elucidates the shared genetic architecture, immunosenescence features, and gut-origin therapeutic targets of ulcerative colitis-associated multisystem inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Enhancing Specificity, Precision, Accessibility, Flexibility, and Safety to Overcome Traditional CRISPR/Cas Editing Challenges and Shape Future Innovations.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Targeted genome-modification tools and their advanced applications in crop breeding.Nature reviews. Genetics · 2024Review
- PRAME induces genomic instability in uveal melanoma.Oncogene · 2024Article
- DNA Glycosylases Define the Outcome of Endogenous Base Modifications.International journal of molecular sciences · 2023Review
- Applications and Prospects of CRISPR/Cas9-Mediated Base Editing in Plant Breeding.Current issues in molecular biology · 2023Review
- Integrated signaling and transcriptome analysis reveals Src family kinase individualities and novel pathways controlled by their constitutive activity.Frontiers in immunology · 2023Article
- Molecular Characterization and Clinical Characteristics of m5C-Based RNA Methylation in Spinal Cord Injury: Validated by qPCR.International journal of genomics · 2022Article
- Interplay between UNG and AID governs intratumoral heterogeneity in mature B cell lymphoma.PLoS genetics · 2020Article
- Article
- The uracil-DNA glycosylase UNG protects the fitness of normal and cancer B cells expressing AID.NAR cancer · 2020Article
- Base Excision Repair in the Immune System: Small DNA Lesions With Big Consequences.Frontiers in immunology · 2020Review
- LMO2 Confers Synthetic Lethality to PARP Inhibition in DLBCL.Cancer cell · 2019Article
- A common SNP in the UNG gene decreases ovarian cancer risk in BRCA2 mutation carriers.Molecular oncology · 2019Article
- Germinal center-derived lymphomas: The darkest side of humoral immunity.Immunological reviews · 2019Review
- Predicting biomedical relationships using the knowledge and graph embedding cascade model.PloS one · 2019Article
- A licensing step links AID to transcription elongation for mutagenesis in B cells.Nature communications · 2018Article
- CD4+ memory T cells infected with latent HIV-1 are susceptible to drugs targeting telomeres.Cell cycle (Georgetown, Tex.) · 2018Article
- Article
- Screening and identification of critical transcription factors involved in the protection of cardiomyocytes against hydrogen peroxide-induced damage by Yixin-shu.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Activation-induced deaminase (AID) initiates antibody gene diversification by creating G:U mismatches in the immunoglobulin loci. However, AID also deaminates nonimmunoglobulin genes, and failure to faithfully repair these off-target lesions can cause B cell lymphoma. In this study, we identify a mechanism by which processing of G:U produced by AID at the telomeres can eliminate B cells at risk of genomic instability. We show that telomeres are off-target substrates of AID and that B cell proliferation depends on protective repair by uracil-DNA glycosylase (UNG). In contrast, in the absence of UNG activity, deleterious processing by mismatch repair leads to telomere loss and defective cell proliferation. Indeed, we show that UNG deficiency reduces B cell clonal expansion in the germinal center in mice and blocks the proliferation of tumor B cells expressing AID. We propose that AID-induced damage at telomeres acts as a fail-safe mechanism to limit the tumor promoting activity of AID when it overwhelms uracil excision repair.
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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.