ArticleProceedings of the National Academy of Sciences of the United States of America2005
A target selection of somatic hypermutations is regulated similarly between T and B cells upon activation-induced cytidine deaminase expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 73 citations in OpenAlex.
- Mutations atMolecular and cellular biology · 2024Article
- B cell-specific knockout of AID protects against atherosclerosis.Scientific reports · 2023Article
- Mutagenic Activity of AID/APOBEC Deaminases in Antiviral Defense and Carcinogenesis.Molecular biology · 2022Article
- Review
- The Common Key to Class-Switch Recombination and Somatic Hypermutation: Discovery of AID and Its Role in Antibody Gene Diversification.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Functions and Malfunctions of Mammalian DNA-Cytosine Deaminases.Chemical reviews · 2016Review
- Genomic Architecture may Influence Recurrent Chromosomal Translocation Frequency in the Igh Locus.Frontiers in immunology · 2013Review
- AID and Apobec3G haphazard deamination and mutational diversity.Cellular and molecular life sciences : CMLS · 2013Review
- Expression of activation-induced cytidine deaminase gene in B lymphocytes of patients with common variable immunodeficiency.Iranian journal of pediatrics · 2013Article
- Article
- Inflammation-mediated genomic instability: roles of activation-induced cytidine deaminase in carcinogenesis.Cancer science · 2012Review
- RAP80 protein is important for genomic stability and is required for stabilizing BRCA1-A complex at DNA damage sites in vivo.The Journal of biological chemistry · 2012Article
- Nonimmunoglobulin target loci of activation-induced cytidine deaminase (AID) share unique features with immunoglobulin genes.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- APOBEC3B can impair genomic stability by inducing base substitutions in genomic DNA in human cells.Scientific reports · 2012Article
- Decrease in topoisomerase I is responsible for activation-induced cytidine deaminase (AID)-dependent somatic hypermutation.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- How does DNA break during chromosomal translocations?Nucleic acids research · 2011Review
- The zebrafish IgH locus contains multiple transcriptional regulatory regions.Developmental and comparative immunology · 2011Article
- Article
- Changes in 2'-deoxycytidine levels in various tissues of tumor-bearing mice.Oncology letters · 2010Article
- Attracting AID to targets of somatic hypermutation.The Journal of experimental medicine · 2010Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Activation-induced cytidine deaminase (AID) is essential for somatic hypermutations (SHM) and class switch recombination. Overexpression of AID in non-B cells can induce SHM in artificial constructs inserted in various loci in the genome. AID overexpression was thus proposed to introduce mutations in a wide variety of genes with little specificity. We previously showed that AID transgenic mice developed T cell lymphomas in which the variable region beta genes of the T cell receptor and c-myc were mutated as frequently as SHM in activated B cells. To understand the target specificity of SHM in AID-expressing T lymphomas, we sequenced six oncogenes (c-myc, pim1, p53, atm, tgfbr-2, and k-ras) and two genes (cd4 and cd5) that are actively transcribed in T lymphomas. SHM was found only in c-myc, pim1, cd4, and cd5, which share the E47 binding motif in the enhancer/promoter. The rest that are not mutated in B cells were not mutated in AID-induced T lymphomas either, although they are transcribed in T and B cells. Comparison of several features of SHM, including selection of targets and mutation distribution, suggests that the regulatory mechanism of SHM is similar between T and B cells. SHM base specificities in the CD4 and CD5 genes were biased to AT, indicating that the preference of target bases of the mutations generated by overexpression of AID is not always GC bases but variable between target genes.
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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.