Evidence map›Paper›PMID 24498102›Full record

ArticlePloS one2014

Acquired deficiency of A20 results in rapid apoptosis, systemic inflammation, and abnormal hematopoietic stem cell function.

Akiko Nagamachi, Yuichiro Nakata, Takeshi Ueda, Norimasa Yamasaki, Yasuhiro Ebihara, Kohichiro Tsuji, Zen-ichiro Honda, Keiyo Takubo, Toshio Suda, Hideaki Oda and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

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  15. Connectivity mapping (ssCMap) to predict A20-inducing drugs and their antiinflammatory action in cystic fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2016
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  16. Recruitment of A20 by the C-terminal domain of NEMO suppresses NF-κB activation and autoinflammatory disease.Proceedings of the National Academy of Sciences of the United States of America · 2016
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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

12 authors at 5 institutions in 1 country.

Akiko NagamachiDepartment of Molecular Oncology, Research Institute of Radiation Biology and Medicine, Hiroshima University, Minami-ku, Hiroshima, Japan.
Yuichiro NakataDepartment of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Minami-ku, Hiroshima, Japan.
Takeshi UedaDepartment of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Minami-ku, Hiroshima, Japan.
Norimasa YamasakiDepartment of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Minami-ku, Hiroshima, Japan.
Yasuhiro EbiharaDivision of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Kohichiro TsujiDivision of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan.
Zen-ichiro HondaHealth Care Center and Graduate School of Humanities and Sciences, Institute of Environmental Science for Human Life, Ochanomizu University, Bunkyo-ku, Tokyo, Japan.
Keiyo TakuboDepartment of Cell Differentiation, The Sakaguchi Laboratory of Developmental Biology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Toshio SudaDepartment of Cell Differentiation, The Sakaguchi Laboratory of Developmental Biology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Hideaki OdaDepartment of Pathology, Tokyo Women's Medical University, Shinjuku-ku, Tokyo, Japan.
Toshiya InabaDepartment of Molecular Oncology, Research Institute of Radiation Biology and Medicine, Hiroshima University, Minami-ku, Hiroshima, Japan.
Hiroaki HondaDepartment of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Minami-ku, Hiroshima, Japan.
Hiroshima University · JPKeio University · JPThe University of Tokyo · JPOchanomizu University · JPTokyo Women's Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A20 is a negative regulator of NF-κB, and mutational loss of A20 expression is involved in the pathogenesis of autoimmune diseases and B-cell lymphomas. To clarify the role of A20 in adult hematopoiesis, we generated conditional A20 knockout mice (A20(flox/flox) ) and crossed them with Mx-1Cre (MxCre (+)) and ERT2Cre (ERT2Cre (+)) transgenic mice in which Cre is inducibly activated by endogenous interferon and exogenous tamoxifen, respectively. A20(flox/flox) MxCre (+) (A20Mx) mice spontaneously exhibited myeloid proliferation, B cell apoptosis, and anemia with overproduction of pro-inflammatory cytokines. Bone marrow transplantation demonstrated that these changes were caused by hematopoietic cells. NF-κB was constitutively activated in A20Mx hematopoietic stem cells (HSCs), which caused enhanced cell cycle entry and impaired repopulating ability. Tamoxifen stimulation of A20(flox/flox) ERT2Cre (+) (A20ERT2) mice induced fulminant apoptosis and subsequent myeloproliferation, lymphocytopenia, and progressive anemia with excessive production of pro-inflammatory cytokines, as observed in A20Mx mice. These results demonstrate that A20 plays essential roles in the homeostasis of adult hematopoiesis by preventing apoptosis and inflammation. Our findings provide insights into the mechanism underlying A20 dysfunction and human diseases in which A20 expression is impaired.

Indexed as

Cell ProliferationAnimalsApoptosisCysteine EndopeptidasesCytokinesDNA-Binding ProteinsHematopoiesisHematopoietic Stem CellsHumansIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutMyeloid CellsNF-kappa BTumor Necrosis Factor alpha-Induced Protein 3Ubiquitin-Protein LigasesCysteine EndopeptidasesCytokinesDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsNF-kappa BTnfaip3 protein, mouseTumor Necrosis Factor alpha-Induced Protein 3Ubiquitin-Protein Ligases

Identifiers

PMID24498102
PMCPMC3909109
OpenAlexW1971893578

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.