Evidence map›Paper›PMID 36324153›Full record

ArticleInflammation and regeneration2022

IL-6 production through repression of UBASH3A gene via epigenetic dysregulation of super-enhancer in CD4

Kaoru Yamagata, Shingo Nakayamada, Tong Zhang, Anh Phuong Nguyen, Naoaki Ohkubo, Shigeru Iwata, Shigeaki Kato, Yoshiya Tanaka

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Inflammation and regeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Aberrant Enhancer Regulation, Phase Separation, and Autoimmune Diseases.Clinical reviews in allergy & immunology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Kaoru YamagataThe First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahata-nishi, Kitakyushu, Fukuoka, 807-8555, Japan.
Shingo NakayamadaThe First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahata-nishi, Kitakyushu, Fukuoka, 807-8555, Japan.
Tong ZhangThe First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahata-nishi, Kitakyushu, Fukuoka, 807-8555, Japan.
Anh Phuong NguyenThe First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahata-nishi, Kitakyushu, Fukuoka, 807-8555, Japan.
Naoaki OhkuboThe First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahata-nishi, Kitakyushu, Fukuoka, 807-8555, Japan.
Shigeru IwataThe First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahata-nishi, Kitakyushu, Fukuoka, 807-8555, Japan.
Shigeaki KatoGraduate School of Life Science and Engineering, Iryo Sosei University, Iwaki, Fukushima, 970-8551, Japan.
Yoshiya TanakaThe First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahata-nishi, Kitakyushu, Fukuoka, 807-8555, Japan. tanaka@med.uoeh-u.ac.jp.ORCID http://orcid.org/0000-0002-0807-7139
University of Occupational and Environmental Health Japan · JPIRYO Sosei University · JP

Funding

Grants-In-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan JSPS KAKENHI #19K08925
6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) is associated with immune dysfunction. UBASH3A as a negative regulator of T cell receptors (TCRs) signaling is a susceptible factor in RA. The aim of this study was to determine the role of UBASH3A in RA pathogenesis, by assessing the role of super-enhancer (SE) in the control of UBASH3A expression in CD4

methodsUBASH3A mRNA and protein levels were quantified by PCR and western blotting, respectively. The cells were treated with a locked nucleic acid to inhibit enhancer RNA (eRNA) expression. Chromatin immunoprecipitation was used to identify the factors recruited to UBASH3A loci displaying SE architecture. CD4

resultsUBASH3A was extracted as a RA susceptibility gene associated with SNPs in the SEs that are highly expressed in CD4

conclusionsIn RA, transcription of UBASH3A is suppressed via epigenetic regulation of SE in CD4

Indexed as

CD4IL-6Rheumatoid arthritisSuper-enhancerUBASH3A

Identifiers

PMID36324153
PMCPMC9632101
OpenAlexW4307986474

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.