Evidence map›Paper›PMID 16477013›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Negative regulation of activation-induced cytidine deaminase in B cells.

Taro Muto, Il-mi Okazaki, Shuichi Yamada, Yoshimasa Tanaka, Kazuo Kinoshita, Masamichi Muramatsu, Hitoshi Nagaoka, Tasuku Honjo

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 94 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Taro MutoDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan.
Il-mi Okazaki
Shuichi Yamada
Yoshimasa Tanaka
Kazuo Kinoshita
Masamichi Muramatsu
Hitoshi Nagaoka
Tasuku Honjo
Kyoto University · JPAkita University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both class switch recombination (CSR) and somatic hypermutation (SHM) of the Ig genes require the activity of activation-induced cytidine deaminase (AID). Expression of AID is restricted to B cells in the germinal centers of the lymphoid organs, where activated B cells undergo CSR and SHM. We previously showed that constitutive and systemic expression of AID leads to tumorigenesis in T cells and lung epithelium, but not in B cells. This finding led us to suspect that transgenic AID may be inactivated at least in part in B cells. To address this issue, we generated conditional AID-transgenic mice that constitutively express AID only in B cells. Studies on the cross between the AID-transgenic and AID-deficient mice showed that abundant AID protein accumulated by constitutive expression is inactivated in B cells, possibly providing an explanation for the absence of deregulation of CSR and SHM in AID-transgenic B cells.

Indexed as

AICDA (Activation-Induced Cytidine Deaminase)AnimalsB-LymphocytesCytidine DeaminaseDown-RegulationImmunoglobulin Class SwitchingMiceMice, TransgenicSomatic Hypermutation, ImmunoglobulinAICDA (Activation-Induced Cytidine Deaminase)Cytidine Deaminase

Identifiers

PMID16477013
PMCPMC1413812
OpenAlexW2147191451

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.