ArticlePhilosophical transactions of the Royal Society of London. Series B, Biological sciences2009
Immunoglobulin class switch recombination: study through human natural mutants.
Article in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 14 citations in OpenAlex.
- AID and Apobec3G haphazard deamination and mutational diversity.Cellular and molecular life sciences : CMLS · 2013Review
- A structural basis for the biochemical behavior of activation-induced deoxycytidine deaminase class-switch recombination-defective hyper-IgM-2 mutants.The Journal of biological chemistry · 2012Article
- B cell TLRs and induction of immunoglobulin class-switch DNA recombination.Frontiers in bioscience (Landmark edition) · 2012Review
- Update on the hyper immunoglobulin M syndromes.British journal of haematology · 2010Review
- Toll-like receptors and B-cell receptors synergize to induce immunoglobulin class-switch DNA recombination: relevance to microbial antibody responses.Critical reviews in immunology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin class switch recombination deficiencies in humans are exquisite models to analyse the mechanisms of class switch recombination (CSR). Besides defects in CD40L/CD40 interaction, others result from an intrinsic B-cell deficiency. The recent elucidation of the molecular basis of some of them has made it possible to delineate the molecular events involved in antibody maturation. Activation-induced (cytidine) deaminase (AID) and uracil-N-glycosylase deficiencies have demonstrated the role of AID as the inducer of DNA lesions in switch and variable regions. However, most of these CSR deficiencies remain molecularly undefined. Their characterization would lead to a better understanding of the complex machinery involved in CSR.
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.