Evidence map›Paper›PMID 11994424›Full record

ArticleThe Journal of experimental medicine2002

The activation-induced deaminase functions in a postcleavage step of the somatic hypermutation process.

F Nina Papavasiliou, David G Schatz

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.7field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
  2. Insights on SNPs of Human Activation-Induced Cytidine Deaminase AID.International journal of molecular sciences · 2025
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

F Nina PapavasiliouLaboratory of Lymphocyte Biology, The Rockefeller University, New York, NY 10021, USA. papavasiliou@rockefeller.edu
David G Schatz
Rockefeller University · USYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of B cells by antigen fuels two distinct molecular modifications of immunoglobulin (Ig) genes. Class-switch recombination (CSR) replaces the Ig(mu) heavy chain constant region with a downstream constant region gene, thereby altering the effector function of the resulting antibodies. Somatic hypermutation (SHM) introduces point mutations into the variable regions of Ig genes, thereby changing the affinity of antibody for antigen. Mechanistic overlap between the two reactions has been suggested by the finding that both require the activation-induced cytidine deaminase (AID). It has been proposed that AID initiates both CSR and SHM by activating a common nuclease. Here we provide evidence that cells lacking AID, or expressing a dominant negative form of the protein, are still able to incur DNA lesions in SHM target sequences. The results indicate that an intact cytidine deaminase motif is required for AID function, and that AID acts downstream of the initial DNA lesions in SHM.

Indexed as

MutagenesisAICDA (Activation-Induced Cytidine Deaminase)Amino Acid SequenceAnimalsB-LymphocytesCytidine DeaminaseImmunoglobulin Constant RegionsImmunoglobulin mu-ChainsMiceMice, KnockoutMolecular Sequence DataPoint MutationRecombination, GeneticReverse Transcriptase Polymerase Chain ReactionAICDA (Activation-Induced Cytidine Deaminase)Cytidine DeaminaseImmunoglobulin Constant RegionsImmunoglobulin mu-Chains

Identifiers

PMID11994424
PMCPMC2193708
OpenAlexW2100736164

What OpenQuestion holds

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LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.