Evidence map›Paper›PMID 38129484›Full record

ArticleScientific reports2023

SET8 is a novel negative regulator of TGF-β signaling in a methylation-independent manner.

Mai Nagasaka, Yasumichi Inoue, Yuji Nagao, Chiharu Miyajima, Daisuke Morishita, Hiromasa Aoki, Mineyoshi Aoyama, Takeshi Imamura, Hidetoshi Hayashi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 39% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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

9 authors at 3 institutions in 1 country.

Mai Nagasaka *Department of Cell Signaling, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, 467-8603, Japan.
Yasumichi Inoue *Department of Cell Signaling, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, 467-8603, Japan. yainoue@phar.nagoya-cu.ac.jp.
Yuji NagaoDepartment of Cell Signaling, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, 467-8603, Japan.
Chiharu MiyajimaDepartment of Cell Signaling, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, 467-8603, Japan.
Daisuke MorishitaDepartment of Cell Signaling, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, 467-8603, Japan.
Hiromasa AokiDepartment of Pathobiology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, 467-8603, Japan.
Mineyoshi AoyamaDepartment of Pathobiology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, 467-8603, Japan.
Takeshi ImamuraDepartment of Molecular Medicine for Pathogenesis, Graduate School of Medicine, Ehime University, Ehime, 791-0295, Japan.
Hidetoshi HayashiDepartment of Cell Signaling, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, 467-8603, Japan. hhayashi@phar.nagoya-cu.ac.jp.
Nagoya City University · JPNagoya University · JPEhime University · JP

Funding

Japan Science and Technology Corporation JPMJSP2130Japan Society for the Promotion of Science 20K07052Japan Society for the Promotion of Science 21H02650Japan Society for the Promotion of Science 23K14389Japan Society for the Promotion of Science 23KJ1818Nagoya City University 2221102
6 · The paper itself

Abstract

Transforming growth factor β (TGF-β) is a multifunctional cytokine that induces a diverse set of cellular processes principally through Smad-dependent transcription. Transcriptional responses induced by Smads are tightly regulated by Smad cofactors and histone modifications; however, the underlying mechanisms have not yet been elucidated in detail. We herein report lysine methyltransferase SET8 as a negative regulator of TGF-β signaling. SET8 physically associates with Smad2/3 and negatively affects transcriptional activation by TGF-β in a catalytic activity-independent manner. The depletion of SET8 results in an increase in TGF-β-induced plasminogen activator inhibitor-1 (PAI-1) and p21 expression and enhances the antiproliferative effects of TGF-β. Mechanistically, SET8 occupies the PAI-1 and p21 promoters, and a treatment with TGF-β triggers the replacement of the suppressive binding of SET8 with p300 on these promoters, possibly to promote gene transcription. Collectively, the present results reveal a novel role for SET8 in the negative regulation of TGF-β signaling.

Indexed as

Plasminogen Activator Inhibitor 1Transforming Growth Factor betaMethylationSignal TransductionSmad2 ProteinTranscriptional ActivationPlasminogen Activator Inhibitor 1Smad2 ProteinTransforming Growth Factor beta

Identifiers

PMID38129484
PMCPMC10739863
OpenAlexW4390050321

What Socratic holds

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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 Socratic graph.