Evidence map›Paper›PMID 27053161›Full record

ArticleNature communications2016

Akt1-mediated Gata3 phosphorylation controls the repression of IFNγ in memory-type Th2 cells.

Hiroyuki Hosokawa, Tomoaki Tanaka, Yusuke Endo, Miki Kato, Kenta Shinoda, Akane Suzuki, Shinichiro Motohashi, Masaki Matsumoto, Keiichi I Nakayama, Toshinori Nakayama

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

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  4. Roles of naïve CD4Journal of translational medicine · 2024
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  7. 14-3-3τ drives estrogen receptor loss via ERα36 induction and GATA3 inhibition in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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  13. Review
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  16. Article
  17. Review
  18. Article
  19. Article
  20. Cytokines, Transcription Factors, and the Initiation of T-Cell Development.Cold Spring Harbor perspectives in biology · 2018
    Review
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

10 authors at 2 institutions in 1 country.

Hiroyuki HosokawaDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
Tomoaki TanakaDepartment of Clinical Cell Biology &Medicine, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.ORCID http://orcid.org/0000-0002-9761-1750
Yusuke EndoDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
Miki KatoDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
Kenta ShinodaDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
Akane SuzukiDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
Shinichiro MotohashiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
Masaki MatsumotoDepartment of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Keiichi I NakayamaDepartment of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Toshinori NakayamaDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
Chiba University · JPKyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Th2 cells produce Th2 cytokines such as IL-4, IL-5 and IL-13, but repress Th1 cytokine IFNγ. Recent studies have revealed various distinct memory-type Th2 cell subsets, one of which produces a substantial amount of IFNγ in addition to Th2 cytokines, however it remains unclear precisely how these Th2 cells produce IFNγ. We herein show that phosphorylation of Gata3 at Ser308, Thr315 and Ser316 induces dissociation of a histone deacetylase Hdac2 from the Gata3/Chd4 repressive complex in Th2 cells. We also identify Akt1 as a Gata3-phosphorylating kinase, and the activation of Akt1 induces derepression of Tbx21 and Ifng expression in Th2 cells. Moreover, T-bet-dependent IFNγ expression in IFNγ-producing memory Th2 cells appears to be controlled by the phosphorylation status of Gata3 in human and murine systems. Thus, this study highlights the molecular basis for posttranslational modifications of Gata3 that control the regulation of IFNγ expression in memory Th2 cells.

Indexed as

Immunologic MemoryAmino Acid SequenceAnimalsEnzyme ActivationFemaleGATA3 Transcription FactorHistone Deacetylase 2HumansInterferon-gammaInterleukin-4MiceMolecular Sequence DataPhosphorylationProto-Oncogene Proteins c-aktT-bet Transcription FactorT-Box Domain ProteinsGATA3 Transcription FactorHDAC2 protein, humanHistone Deacetylase 2Interferon-gammaInterleukin-4Proto-Oncogene Proteins c-aktT-bet Transcription FactorT-Box Domain Proteins

Identifiers

PMID27053161
PMCPMC4829694
OpenAlexW2324150637

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.