ReviewCellular and molecular life sciences : CMLS2013
AID and Apobec3G haphazard deamination and mutational diversity.
Review in Cellular and molecular life sciences : CMLS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed.
- Review
- Random Walk Enzymes: Information Theory, Quantum Isomorphism, and Entropy Dispersion.The journal of physical chemistry. A · 2019Article
- Mutations in human AID differentially affect its ability to deaminate cytidine and 5-methylcytidine in ssDNA substrates in vitro.Scientific reports · 2017Article
- Deoxyinosine triphosphate induces MLH1/PMS2- and p53-dependent cell growth arrest and DNA instability in mammalian cells.Scientific reports · 2016Article
- Clustered mutations in hominid genome evolution are consistent with APOBEC3G enzymatic activity.Genome research · 2016Article
- Activation-induced deoxycytidine deaminase (AID) co-transcriptional scanning at single-molecule resolution.Nature communications · 2015Article
- Characterization of the Catalytic Domain of Human APOBEC3B and the Critical Structural Role for a Conserved Methionine.Journal of molecular biology · 2015Article
- Random-walk enzymes.Physical review. E, Statistical, nonlinear, and soft matter physics · 2015Article
- Molecular targets and pathways involved in liver metastasis of colorectal cancer.Clinical & experimental metastasis · 2015Review
- High-throughput mutagenesis reveals functional determinants for DNA targeting by activation-induced deaminase.Nucleic acids research · 2014Article
- Tautomerism provides a molecular explanation for the mutagenic properties of the anti-HIV nucleoside 5-aza-5,6-dihydro-2'-deoxycytidine.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Mismatch repair proteins and AID activity are required for the dominant negative function of C-terminally deleted AID in class switching.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Base excision repair: a critical player in many games.DNA repair · 2014Review
- Structural determinants of human APOBEC3A enzymatic and nucleic acid binding properties.Nucleic acids research · 2014Article
- A mathematical model for scanning and catalysis on single-stranded DNA, illustrated with activation-induced deoxycytidine deaminase.The Journal of biological chemistry · 2013Article
- A biochemical analysis linking APOBEC3A to disparate HIV-1 restriction and skin cancer.The Journal of biological chemistry · 2013Article
- Fate mapping for activation-induced cytidine deaminase (AID) marks non-lymphoid cells during mouse development.PloS one · 2013Article
- The multifaceted roles of RNA binding in APOBEC cytidine deaminase functions.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Activation-induced deoxycytidine deaminase (AID) and Apobec 3G (Apo3G) cause mutational diversity by initiating mutations on regions of single-stranded (ss) DNA. Expressed in B cells, AID deaminates C → U in actively transcribed immunoglobulin (Ig) variable and switch regions to initiate the somatic hypermutation (SHM) and class switch recombination (CSR) that are essential for antibody diversity. Apo3G expressed in T cells catalyzes C deaminations on reverse transcribed cDNA causing HIV-1 retroviral inactivation. When operating properly, AID- and Apo3G-initiated mutations boost human fitness. Yet, both enzymes are potentially powerful somatic cell "mutators". Loss of regulated expression and proper genome targeting can cause human cancer. Here, we review well-established biological roles of AID and Apo3G. We provide a synopsis of AID partnering proteins during SHM and CSR, and describe how an Apo2 crystal structure provides "surrogate" insight for AID and Apo3G biochemical behavior. However, large gaps remain in our understanding of how dC deaminases search ssDNA to identify trinucleotide motifs to deaminate. We discuss two recent methods to analyze ssDNA scanning and deamination. Apo3G scanning and deamination is visualized in real-time using single-molecule FRET, and AID deamination efficiencies are determined with a random walk analysis. AID and Apo3G encounter many candidate deamination sites while scanning ssDNA. Generating mutational diversity is a principal aim of AID and an important ancillary property of Apo3G. Success seems likely to involve hit and miss deamination motif targeting, biased strongly toward miss.
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Registered trials
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