ArticleNature2013
AID stabilizes stem-cell phenotype by removing epigenetic memory of pluripotency genes.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Evolutionary Comparative Analyses of DNA-Editing Enzymes of the Immune System: From 5-Dimensional Description of Protein Structures to Immunological Insights and Applications to Protein Engineering.Frontiers in immunology · 2021Pooled it
- Activation-induced cytidine deaminase in tertiary lymphoid structures: dual roles and implications in cancer prognosis.Frontiers in oncology · 2025Review
- Hepatocyte Smoothened Activity Controls Susceptibility to Insulin Resistance and Nonalcoholic Fatty Liver Disease.Cellular and molecular gastroenterology and hepatology · 2023Article
- Aberrant APOBEC3C expression induces characteristic genomic instability in pancreatic ductal adenocarcinoma.Oncogenesis · 2022Article
- Review
- CancerFrontiers in immunology · 2021Article
- Genetic and epigenetic determinants of diffuse large B-cell lymphoma.Blood cancer journal · 2020Review
- Optimized high-fidelity 3DPCR to assess potential mitochondrial targeting by activation-induced cytidine deaminase.FEBS open bio · 2020Article
- Activation-Induced Cytidine Deaminase Regulates Fibroblast Growth Factor/Extracellular Signal-Regulated Kinases Signaling to Achieve the Naïve Pluripotent State During Reprogramming.Stem cells (Dayton, Ohio) · 2019Article
- Activation-induced deaminase (AID) localizes to the nucleus in brief pulses.PLoS genetics · 2019Article
- Epigenetics of metabolic syndrome.Physiological genomics · 2018Review
- Understanding the Structure, Multimerization, Subcellular Localization and mC Selectivity of a Genomic Mutator and Anti-HIV Factor APOBEC3H.Scientific reports · 2018Article
- Epigenomic Modifications Mediating Antibody Maturation.Frontiers in immunology · 2018Review
- Mutations in human AID differentially affect its ability to deaminate cytidine and 5-methylcytidine in ssDNA substrates in vitro.Scientific reports · 2017Article
- Family-Wide Comparative Analysis of Cytidine and Methylcytidine Deamination by Eleven Human APOBEC Proteins.Journal of molecular biology · 2017Article
- Article
- Cutting Edge: The Transcription Factor Sox2 Regulates AID Expression in Class-Switched B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Gender Differences in Global but Not Targeted Demethylation in iPSC Reprogramming.Cell reports · 2017Article
- Skeletal Muscle Cell Induction from Pluripotent Stem Cells.Stem cells international · 2017Review
- Activation-induced cytidine deaminase selectively catalyzed active DNA demethylation in pluripotency gene and improved cell reprogramming in bovine SCNT embryo.Cytotechnology · 2016Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
The activation-induced cytidine deaminase (AID; also known as AICDA) enzyme is required for somatic hypermutation and class switch recombination at the immunoglobulin locus. In germinal-centre B cells, AID is highly expressed, and has an inherent mutator activity that helps generate antibody diversity. However, AID may also regulate gene expression epigenetically by directly deaminating 5-methylcytosine in concert with base-excision repair to exchange cytosine. This pathway promotes gene demethylation, thereby removing epigenetic memory. For example, AID promotes active demethylation of the genome in primordial germ cells. However, different studies have suggested either a requirement or a lack of function for AID in promoting pluripotency in somatic nuclei after fusion with embryonic stem cells. Here we tested directly whether AID regulates epigenetic memory by comparing the relative ability of cells lacking AID to reprogram from a differentiated murine cell type to an induced pluripotent stem cell. We show that Aid-null cells are transiently hyper-responsive to the reprogramming process. Although they initiate expression of pluripotency genes, they fail to stabilize in the pluripotent state. The genome of Aid-null cells remains hypermethylated in reprogramming cells, and hypermethylated genes associated with pluripotency fail to be stably upregulated, including many MYC target genes. Recent studies identified a late step of reprogramming associated with methylation status, and implicated a secondary set of pluripotency network components. AID regulates this late step, removing epigenetic memory to stabilize the pluripotent state.
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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.