ArticleProceedings of the National Academy of Sciences of the United States of America2002
AID-GFP chimeric protein increases hypermutation of Ig genes with no evidence of nuclear localization.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
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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
49 citing papers in PubMed, 126 citations in OpenAlex.
- B cell receptor stimulation inhibits class switch recombination through elevated DNA repair.DNA repair · 2026Article
- In vitro affinity maturation of broader and more-potent variants of the HIV-1-neutralizing antibody CAP256-VRC26.25.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- AID in Chronic Lymphocytic Leukemia: Induction and Action During Disease Progression.Frontiers in oncology · 2021Review
- Article
- Transcription factor binding at Ig enhancers is linked to somatic hypermutation targeting.European journal of immunology · 2020Article
- A Protein Antagonist of Activation-Induced Cytidine Deaminase Encoded by a Complex Mouse Retrovirus.mBio · 2019Article
- Activation-induced deaminase (AID) localizes to the nucleus in brief pulses.PLoS genetics · 2019Article
- Transcription factor YY1 can control AID-mediated mutagenesis in mice.European journal of immunology · 2018Article
- Diversity in the Cow Ultralong CDR H3 Antibody Repertoire.Frontiers in immunology · 2018Review
- Application of Stem Cells in Oral Disease Therapy: Progresses and Perspectives.Frontiers in physiology · 2017Review
- Activation-Induced Cytidine Deaminase Expression in Human B Cell Precursors Is Essential for Central B Cell Tolerance.Immunity · 2015Article
- Cell Cycle Regulates Nuclear Stability of AID and Determines the Cellular Response to AID.PLoS genetics · 2015Article
- Consecutive interactions with HSP90 and eEF1A underlie a functional maturation and storage pathway of AID in the cytoplasm.The Journal of experimental medicine · 2015Article
- Generation and characterization of induced pluripotent stem cells from Aid-deficient mice.PloS one · 2014Article
- Regulation of immunoglobulin class-switch recombination: choreography of noncoding transcription, targeted DNA deamination, and long-range DNA repair.Advances in immunology · 2014Review
- Evidence for APOBEC3B mutagenesis in multiple human cancers.Nature genetics · 2013Article
- Role of activation-induced cytidine deaminase in the development of oral squamous cell carcinoma.PloS one · 2013Article
- Etoposide induces nuclear re-localisation of AID.PloS one · 2013Article
- The role of cytidine deaminases on innate immune responses against human viral infections.BioMed research international · 2013Review
- A role for the RNA pol II-associated PAF complex in AID-induced immune diversification.The Journal of experimental medicine · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic hypermutation generates variants of antibody genes and underpins the affinity maturation of antibodies. It is restricted to the V-gene segments, and although it decays exponentially toward the 3'end, it includes recognizable hot spots. Although the detailed mechanism of hypermutation remains elusive, the process may take place in two separate stages, preferentially targeting G/Cs in the first and A/Ts in the second stage. It seems that MSH2 is involved in the second stage, and that activation induced deaminase (AID) is implicated in the control of hypermutation. The constitutively hypermutating cell line Ramos expresses AID, and we have prepared transfectants that express a chimeric AID-green fluorescent protein. The fluorescence is strongly detected in the cytoplasm but not in the nucleus. Yet, the chimeric protein increases the hypermutation rate either directly or, more likely, indirectly, by favoring the transport of AID into the nucleus. Thus, in Ramos, AID seems to be rate limiting. Unexpectedly, the proportion of deletions also is increased. The increase in mutation rate detected by a fast cytofluorimetric method based on the accumulation of sIgM-loss mutants correlates with the increase measured by mutations defined by sequence analysis. The higher mutation rate is largely explained by the higher proportion of mutated clones, indicating that AID controls the number of cells that undergo hypermutation but not the number of mutations that are incorporated in each mutation round.
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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.