ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Multiple transcription factor binding sites predict AID targeting in non-Ig genes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 35 citations in OpenAlex.
- Activation-induced cytidine deaminase (AID) suppresses the activity of HBV EnhII/CP by downregulating FANCE expression.Virus genes · 2026Article
- Mechanism and regulation of secondary immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2023Review
- BTG1 inactivation drives lymphomagenesis and promotes lymphoma dissemination through activation of BCAR1.Blood · 2023Article
- Association of mutation signature effectuating processes with mutation hotspots in driver genes and non-coding regions.Nature communications · 2022Article
- Roles of Bone Morphogenetic Protein Receptor 1A in Germinal Centers and Long-Lived Humoral Immunity.ImmunoHorizons · 2021Article
- AID assists DNMT1 to attenuate BCL6 expression through DNA methylation in diffuse large B-cell lymphoma cell lines.Neoplasia (New York, N.Y.) · 2020Article
- The RNA-binding protein ROD1/PTBP3 cotranscriptionally defines AID-loading sites to mediate antibody class switch in mammalian genomes.Cell research · 2018Article
- Epigenomic Modifications Mediating Antibody Maturation.Frontiers in immunology · 2018Review
- AID Recognizes Structured DNA for Class Switch Recombination.Molecular cell · 2017Article
- Diffuse large B-cell lymphoma: can genomics improve treatment options for a curable cancer?Cold Spring Harbor molecular case studies · 2017Review
- Defining chromosomal translocation risks in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- YY1 Is Required for Germinal Center B Cell Development.PloS one · 2016Article
- Practical guidelines for B-cell receptor repertoire sequencing analysis.Genome medicine · 2015Review
- IL-21-driven neoplasms in SJL mice mimic some key features of human angioimmunoblastic T-cell lymphoma.The American journal of pathology · 2015Article
- AID targeting: old mysteries and new challenges.Trends in immunology · 2015Review
- Nbs1 ChIP-Seq Identifies Off-Target DNA Double-Strand Breaks Induced by AID in Activated Splenic B Cells.PLoS genetics · 2015Article
- Related Mechanisms of Antibody Somatic Hypermutation and Class Switch Recombination.Microbiology spectrum · 2015Review
- Convergent transcription at intragenic super-enhancers targets AID-initiated genomic instability.Cell · 2014Article
- Targeting of somatic hypermutation by immunoglobulin enhancer and enhancer-like sequences.PLoS biology · 2014Article
- Function of YY1 in Long-Distance DNA Interactions.Frontiers in immunology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Aberrant targeting of the enzyme activation-induced cytidine deaminase (AID) results in the accumulation of somatic mutations in ≈ 25% of expressed genes in germinal center B cells. Observations in Ung(-/-) Msh2(-/-) mice suggest that many other genes efficiently repair AID-induced lesions, so that up to 45% of genes may actually be targeted by AID. It is important to understand the mechanisms that recruit AID to certain genes, because this mistargeting represents an important risk for genome instability. We hypothesize that several mechanisms combine to target AID to each locus. To resolve which mechanisms affect AID targeting, we analyzed 7.3 Mb of sequence data, along with the regulatory context, from 83 genes in Ung(-/-) Msh2(-/-) mice to identify common properties of AID targets. This analysis identifies three transcription factor binding sites (E-box motifs, along with YY1 and C/EBP-β binding sites) that may work together to recruit AID. Based on previous knowledge and these newly discovered features, a classification tree model was built to predict genome-wide AID targeting. Using this predictive model, we were able to identify a set of 101 high-interest genes that are likely targets of AID.
Indexed as
Identifiers
What 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.