Evidence map›Paper›PMID 28400474›Full record

ArticleThe Journal of experimental medicine2017

Suppression of Th17 cell differentiation by misshapen/NIK-related kinase MINK1.

Guotong Fu, Qin Xu, Yuanjun Qiu, Xuexiao Jin, Ting Xu, Shunli Dong, Jianli Wang, Yuehai Ke, Hu Hu, Xuetao Cao and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

47 citing papers in PubMed, 61 citations in OpenAlex.

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  12. Application of Antioxidant Compounds in Bone Defect Repair.Antioxidants (Basel, Switzerland) · 2024
    Review
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  18. The PRAK-NRF2 axis promotes the differentiation of Th17 cells by mediating the redox homeostasis and glycolysis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 2 countries.

Guotong FuInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China.
Qin XuInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China.
Yuanjun QiuInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China.
Xuexiao JinInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China.
Ting XuInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China.
Shunli DongLife Sciences Institute, Zhejiang University, Hangzhou 310058, China.
Jianli WangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China.ORCID 0000-0001-8154-3063
Yuehai KeProgram in Molecular and Cellular Biology, Zhejiang University School of Medicine, Hangzhou 310058, China.
Hu HuDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, Hangzhou 310058, China.
Xuetao CaoInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China.
Di WangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China.
Harvey CantorDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.
Xiang GaoKey Laboratory of Model Animals for Disease Study of the Ministry of Education, Model Animal Research Center, Nanjing University, Nanjing 210061, China.
Linrong LuInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China lu_linrong@zju.edu.cn.ORCID 0000-0002-0171-4115
Zhejiang University · CNHarvard University · USModel Animal Research Center · CNSecond Military Medical University · CNZhejiang University-University of Edinburgh Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T helper type 17 cells (Th17 cells) are major contributors to many autoimmune diseases. In this study, we demonstrate that the germinal center kinase family member MINK1 (misshapen/NIK-related kinase 1) negatively regulates Th17 cell differentiation. The suppressive effect of MINK1 on induction of Th17 cells is mediated by the inhibition of SMAD2 activation through direct phosphorylation of SMAD2 at the T324 residue. The importance of MINK1 to Th17 cell differentiation was strengthened in the animal model of experimental autoimmune encephalomyelitis (EAE). Moreover, we show that the reactive oxygen species (ROS) scavenger

Indexed as

AnimalsCell DifferentiationDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalMaleMiceMice, KnockoutProtein Serine-Threonine KinasesReactive Oxygen SpeciesSmad2 ProteinTh17 CellsMINK7 protein, mouseProtein Serine-Threonine KinasesReactive Oxygen SpeciesSmad2 ProteinSmad2 protein, mouse

Identifiers

PMID28400474
PMCPMC5413330
OpenAlexW2607326270

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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.