Evidence map›Paper›PMID 35343079›Full record

ArticleClinical and translational medicine2022

GPR65 promotes intestinal mucosal Th1 and Th17 cell differentiation and gut inflammation through downregulating NUAK2.

Ritian Lin, Wei Wu, Huimin Chen, Han Gao, Xiaohan Wu, Gengfeng Li, Qiong He, Huiying Lu, Mingming Sun, Zhanju Liu

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Persistent CD4Cellular immunology · 2026
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  7. Article
  8. Tuft Cells in the Gut Limit Cognitive Disorders by Regulating Gut Homeostasis.Cellular and molecular gastroenterology and hepatology · 2026
    Article
  9. Article
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  14. Review
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  17. Review
  18. Article
  19. Activation of the proton-sensing GPCR, GPR65 on fibroblast-like synoviocytes contributes to inflammatory joint pain.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Ritian LinCenter for Inflammatory Bowel Disease Research, The Shanghai Tenth People's Hospital, Tongji University of School Medicine, Shanghai, China.ORCID 0000-0003-3867-0061
Wei WuCenter for Inflammatory Bowel Disease Research, The Shanghai Tenth People's Hospital, Tongji University of School Medicine, Shanghai, China.
Huimin ChenCenter for Inflammatory Bowel Disease Research, The Shanghai Tenth People's Hospital, Tongji University of School Medicine, Shanghai, China.
Han GaoCenter for Inflammatory Bowel Disease Research, The Shanghai Tenth People's Hospital, Tongji University of School Medicine, Shanghai, China.
Xiaohan WuCenter for Inflammatory Bowel Disease Research, The Shanghai Tenth People's Hospital, Tongji University of School Medicine, Shanghai, China.
Gengfeng LiCenter for Inflammatory Bowel Disease Research, The Shanghai Tenth People's Hospital, Tongji University of School Medicine, Shanghai, China.
Qiong HeCenter for Inflammatory Bowel Disease Research, The Shanghai Tenth People's Hospital, Tongji University of School Medicine, Shanghai, China.
Huiying LuCenter for Inflammatory Bowel Disease Research, The Shanghai Tenth People's Hospital, Tongji University of School Medicine, Shanghai, China.
Mingming SunCenter for Inflammatory Bowel Disease Research, The Shanghai Tenth People's Hospital, Tongji University of School Medicine, Shanghai, China.
Zhanju LiuCenter for Inflammatory Bowel Disease Research, The Shanghai Tenth People's Hospital, Tongji University of School Medicine, Shanghai, China.ORCID 0000-0002-0326-543X
Tongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G protein-coupled receptor 65 (GPR65), a susceptibility gene for inflammatory bowel diseases (IBD), has been identified to promote Th17 cell pathogenicity and induce T cell apoptosis. However, the potential role of GPR65 in modulating CD4

Indexed as

Th17 CellsTh1 CellsAnimalsCell DifferentiationHumansInflammationIntestinal MucosaMiceProtein Serine-Threonine KinasesReceptors, G-Protein-CoupledGPR65 protein, humanGPR65 protein, mouseNUAK2 protein, humanProtein Serine-Threonine KinasesReceptors, G-Protein-CoupledGPR65inflammatory bowel diseasesTh17 cellsTh1 cells

Identifiers

PMID35343079
PMCPMC8958354
OpenAlexW4220700693

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.