Evidence map›Paper›PMID 19966806›Full record

ArticleNature immunology2010

B cell-specific and stimulation-responsive enhancers derepress Aicda by overcoming the effects of silencers.

Thinh Huy Tran, Mikiyo Nakata, Keiichiro Suzuki, Nasim A Begum, Reiko Shinkura, Sidonia Fagarasan, Tasuku Honjo, Hitoshi Nagaoka

Open access · bronzeAbstract read
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In one paragraph

Article in Nature immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

74 citing papers in PubMed, 122 citations in OpenAlex.

  1. Trial
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  5. The LIM-domain-only protein LMO2 and its binding partner LDB1 are differentially required for class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  18. Activation-induced cytidine deaminase: in sickness and in health.Journal of cancer research and clinical oncology · 2020
    Review
  19. Article
  20. Article

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Thinh Huy TranDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan. honjo@mfour.med.kyoto-u.ac.jp
Mikiyo Nakata
Keiichiro Suzuki
Nasim A Begum
Reiko Shinkura
Sidonia Fagarasan
Tasuku Honjo
Hitoshi Nagaoka
Kyoto University · JPRIKEN · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation-induced cytidine deaminase (AID) is essential for the generation of antibody memory but also targets oncogenes, among other genes. We investigated the transcriptional regulation of Aicda (which encodes AID) in class switch-inducible CH12F3-2 cells and found that Aicda regulation involved derepression by several layers of positive regulatory elements in addition to the 5' promoter region. The 5' upstream region contained functional motifs for the response to signaling by cytokines, the ligand for the costimulatory molecule CD40 or stimuli that activated the transcription factor NF-kappaB. The first intron contained functional binding elements for the ubiquitous silencers c-Myb and E2f and for the B cell-specific activator Pax5 and E-box-binding proteins. Our results show that Aicda is regulated by the balance between B cell-specific and stimulation-responsive elements and ubiquitous silencers.

Indexed as

AICDA (Activation-Induced Cytidine Deaminase)AnimalsB-LymphocytesCytidine DeaminaseEnhancer Elements, GeneticGene ExpressionGene Expression ProfilingGene Expression RegulationGenes, ImmunoglobulinHumansImmunoglobulin Class SwitchingImmunologic MemoryMiceMutagenesis, Site-DirectedOligonucleotide Array Sequence AnalysisOncogenesAICDA (Activation-Induced Cytidine Deaminase)Cytidine Deaminase

Identifiers

PMID19966806
OpenAlexW2128410841

What OpenQuestion holds

Textmetadata
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.