Evidence map›Paper›PMID 29483615›Full record

ArticleGenes and immunity2019

CRISPR/cas9 mediated knockout of an intergenic variant rs6927172 identified IL-20RA as a new risk gene for multiple autoimmune diseases.

Jianfeng Wu, Sirui Yang, Di Yu, Wenjing Gao, Xianjun Liu, Kun Zhang, Xueqi Fu, Wanguo Bao, Kaiyu Zhang, Jiaao Yu and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Genes and immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
1.8field-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

19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.

  1. Pooled it
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  12. Functional genomics in autoimmune diseases.Human molecular genetics · 2020
    Review
  13. Article
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  15. Message from the new Editors-in-Chief.Genes and immunity · 2019
    Article
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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 1 institution in 1 country.

Jianfeng Wu *The Institute of Epigenetic Medicine, The First Hospital of Jilin University, Changchun, China.
Sirui Yang *The Institute of Pediatrics, The First Hospital of Jilin University, Changchun, China.
Di YuThe Institute of Epigenetic Medicine, The First Hospital of Jilin University, Changchun, China.
Wenjing GaoThe Institute of Epigenetic Medicine, The First Hospital of Jilin University, Changchun, China.
Xianjun LiuThe Institute of Epigenetic Medicine, The First Hospital of Jilin University, Changchun, China.
Kun ZhangThe Center of Research, The Second Hospital of Jilin University, Changchun, China.
Xueqi FuThe College of Life Sciences, The Jilin University, Changchun, China.
Wanguo BaoDepartment of Infectious Diseases, The First Hospital of Jilin University, Changchun, China.
Kaiyu ZhangDepartment of Infectious Diseases, The First Hospital of Jilin University, Changchun, China.
Jiaao YuDepartment of Burn Surgery, The First Hospital of Jilin University, Changchun, China.
Liankun SunCollege of Basic Medicine, The Jilin University, Changchun, China.
Shaofeng WangThe Institute of Epigenetic Medicine, The First Hospital of Jilin University, Changchun, China. shaofengwang@jlu.edu.cn.ORCID http://orcid.org/0000-0001-8314-7304
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic variants near the tumor necrosis factor-α-induced protein 3 gene (TNFAIP3) at the chromosomal region 6q23 demonstrated significant associations with multiple autoimmune diseases. The signals of associations have been explained to the TNFAIP3 gene, the most likely causal gene. In this study, we employed CRISPR/cas9 genome-editing tool to generate cell lines with deletions including a candidate causal variant, rs6927172, at 140 kb upstream of the TNFAIP3 gene. Interestingly, we observed alterations of multiple genes including IL-20RA encoding a subunit of the receptor for interleukin 20. Using Electrophoretic mobility shift assay (EMSA), Western blotting, and chromatin conformation capture we characterized the molecular mechanism that the DNA element carrying the variant rs6927172 influences expression of IL-20RA and TNFAIP3 genes. Additionally, we developed a new use of the transcription activator-like effector (TALE) to study the role of the variant in regulating expressions of its target genes. In summary, we generated deletion knockouts that included the candidate causal variant rs6927172 in HEK293T cells provided new evidence and mechanism for IL-20RA gene as a risk factor for multiple autoimmune diseases.

Indexed as

Polymorphism, Single NucleotideAutoimmune DiseasesCRISPR-Cas SystemsHEK293 CellsHumansMutationReceptors, InterleukinTumor Necrosis Factor alpha-Induced Protein 3interleukin-20 receptorReceptors, InterleukinTNFAIP3 protein, humanTumor Necrosis Factor alpha-Induced Protein 3

Identifiers

PMID29483615
OpenAlexW2791430023

What OpenQuestion holds

Textmetadata
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.