Evidence map›Paper›PMID 20100870›Full record

ArticleThe Journal of experimental medicine2010

Attracting AID to targets of somatic hypermutation.

Atsushi Tanaka, Hong Ming Shen, Sarayu Ratnam, Prashant Kodgire, Ursula Storb

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  4. Review
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  7. Article
  8. Class-Switch Recombination in the Absence of the IgH 3' Regulatory Region.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. AID and Apobec3G haphazard deamination and mutational diversity.Cellular and molecular life sciences : CMLS · 2013
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Identification of core DNA elements that target somatic hypermutation.Journal of immunology (Baltimore, Md. : 1950) · 2012
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Atsushi TanakaCommittee on Immunology, University of Chicago, Chicago, IL 60637, USA.
Hong Ming Shen
Sarayu Ratnam
Prashant Kodgire
Ursula Storb
University of Chicago · US

Funding

MECHANISM OF IMMUNOGLOBULIN HYPERMUTATIONR01AI047380 · NIAID · UNIVERSITY OF CHICAGO · PI STORB, URSULA B · 2000 to 2010
$4.2M
Immunoglobulin Somatic MutationR01AI053130 · NIAID · UNIVERSITY OF CHICAGO · PI STORB, URSULA B · 2003 to 2007
$1.3M
Mechanism of Immunoglobulin HypermutationR56AI047380 · NIAID · UNIVERSITY OF CHICAGO · PI STORB, URSULA B · 2012 to 2012
$395k
NIAID NIH HHS AI047380NIAID NIH HHS AI053130NIAID NIH HHS R01 AI047380NIAID NIH HHS R01 AI053130NIAID NIH HHS R56 AI047380
6 · The paper itself

Abstract

The process of somatic hypermutation (SHM) of immunoglobulin (Ig) genes requires activation-induced cytidine deaminase (AID). Although mistargeting of AID is detrimental to genome integrity, the mechanism and the cis-elements responsible for targeting of AID are largely unknown. We show that three CAGGTG cis-elements in the context of Ig enhancers are sufficient to target SHM to a nearby transcribed gene. The CAGGTG motif binds E47 in nuclear extracts of the mutating cells. Replacing CAGGTG with AAGGTG in the construct without any other E47 binding site eliminates SHM. The CA versus AA effect requires AID. CAGGTG does not enhance transcription, chromatin acetylation, or overall target gene activity. The other cis-elements of Ig enhancers alone cannot attract the SHM machinery. Collectively with other recent findings, we postulate that AID targets all genes expressed in mutating B cells that are associated with CAGGTG motifs in the appropriate context. Ig genes are the most highly mutated genes, presumably because of multiple CAGGTG motifs within the Ig genes, high transcription activity, and the presence of other cooperating elements in Ig enhancers.

Indexed as

Cytidine DeaminaseGenes, ImmunoglobulinSomatic Hypermutation, ImmunoglobulinAnimalsBase SequenceBinding SitesB-LymphocytesCell LineChickensEnhancer Elements, GeneticEnzyme ActivationMutationTCF Transcription FactorsTranscription Factor 7-Like 1 ProteinTranscription, GeneticCytidine DeaminaseTCF Transcription FactorsTranscription Factor 7-Like 1 Protein

Identifiers

PMID20100870
PMCPMC2822603
OpenAlexW2127875677

What OpenQuestion holds

Textmetadata
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.