Evidence map›Paper›PMID 28598443›Full record

ArticleNature communications2017

Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity.

Meng Xia, Juan Liu, Shuxun Liu, Kun Chen, Hongyu Lin, Minghong Jiang, Xiaoqing Xu, Yiquan Xue, Wei Liu, Yan Gu and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 15% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. LNCing RNA to immunity.Trends in immunology · 2022
    Review
  18. LncRNA-mediated DNA methylation: an emerging mechanism in cancer and beyond.Journal of experimental & clinical cancer research : CR · 2022
    Review
  19. Review
  20. 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

19 authors at 5 institutions in 1 country.

Meng XiaNational Key Laboratory of Medical Molecular Biology, Department of Immunology &Center for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China.
Juan LiuNational Key Laboratory of Medical Immunology &Institute of Immunology, Second Military Medical University, Shanghai 200433, China.
Shuxun LiuNational Key Laboratory of Medical Immunology &Institute of Immunology, Second Military Medical University, Shanghai 200433, China.
Kun ChenInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China.
Hongyu LinInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China.
Minghong JiangNational Key Laboratory of Medical Molecular Biology, Department of Immunology &Center for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China.
Xiaoqing XuNational Key Laboratory of Medical Molecular Biology, Department of Immunology &Center for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China.
Yiquan XueNational Key Laboratory of Medical Immunology &Institute of Immunology, Second Military Medical University, Shanghai 200433, China.
Wei LiuNational Key Laboratory of Medical Molecular Biology, Department of Immunology &Center for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China.
Yan GuNational Key Laboratory of Medical Immunology &Institute of Immunology, Second Military Medical University, Shanghai 200433, China.
Xiang ZhangNational Key Laboratory of Medical Immunology &Institute of Immunology, Second Military Medical University, Shanghai 200433, China.
Zhiqing LiInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China.
Lin YiNational Key Laboratory of Medical Immunology &Institute of Immunology, Second Military Medical University, Shanghai 200433, China.
Youcun QianInstitute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200025, China.
Chen ZhouDepartment of Rheumatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100032, China.
Ru LiDepartment of Rheumatology &Immunology, Peking University People's Hospital, Beijing 100044, China.
Xuan ZhangDepartment of Rheumatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100032, China.ORCID 0000-0001-8775-1699
Zhanguo LiDepartment of Rheumatology &Immunology, Peking University People's Hospital, Beijing 100044, China.
Xuetao CaoNational Key Laboratory of Medical Molecular Biology, Department of Immunology &Center for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China.
Second Military Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University · CNZhejiang University · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulatory T (Treg) cells are important for the maintenance of immune homoeostasis and prevention of autoimmune diseases. Epigenetic modifications have been reported to modulate autoimmunity by altering Treg cell fate. Here we show that the H3K4 methyltransferase Ash1l facilitates TGF-β-induced Treg cell polarization in vitro and protects mice from T cell-mediated colitis in vivo. Ash1l upregulates Smad3 expression by directly targeting Smad3 promoter to increase local H3K4 trimethylation. Furthermore, we identify an lncRNA, namely lnc-Smad3, which interacts with the histone deacetylase HDAC1 and silences Smad3 transcription. After TGF-β stimulation, activated Smad3 suppresses lnc-Smad3 transcription, thereby recovering the Smad3 promoter accessibility to Ash1l. By revealing the opposite regulatory functions of Ash1l and lnc-Smad3 in Smad3 expression, our data provide insights for the epigenetic control of Treg cell fate to potentially aid in the development of therapeutic intervention for autoimmune diseases.

Indexed as

AutoimmunityCell PolarityAdultAgedAnimalsDNA-Binding ProteinsEpigenesis, GeneticGene Expression RegulationGene SilencingHistone Deacetylase 1Histone-Lysine N-MethyltransferaseHistonesHumansMethylationMiceMice, Inbred C57BLASH1L protein, humanAsh1l protein, mouseDNA-Binding ProteinsHistone Deacetylase 1Histone-Lysine N-MethyltransferaseHistonesRNA, Long NoncodingSmad3 ProteinTranscription FactorsTransforming Growth Factor beta

Identifiers

PMID28598443
PMCPMC5472765
OpenAlexW2624182835

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.