Evidence map›Paper›PMID 42017384›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Epithelial TRIM27 Inhibits Intestinal Inflammation in Ulcerative Colitis by the USP7/TRIM27-IKK Double Negative-Feedback.

Weimin Xu, Zhebin Hua, Zhujiang Dai, Shasha Zhang, Yihan Jiang, Wensong Ge, YingWei Chen, Zhongchuan Wang, Bing Zhang, Chen-Ying Liu and 1 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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0citing papers in PubMed
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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Weimin XuDepartment of Colorectal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Zhebin HuaDepartment of Colorectal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Zhujiang DaiDepartment of Colorectal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Shasha ZhangKey Laboratory of Systems Biomedicine, Shanghai Center for Systems Biomedicine, Shanghai, China.
Yihan JiangKeck School of Medicine, University of Southern California, Los Angeles, California, USA.
Wensong GeDepartment of Gastroenterology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
YingWei ChenDepartment of Gastroenterology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Zhongchuan WangDepartment of Colorectal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Bing ZhangKey Laboratory of Systems Biomedicine, Shanghai Center for Systems Biomedicine, Shanghai, China.
Chen-Ying LiuDepartment of Colorectal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Peng DuDepartment of Colorectal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0001-9355-0789

Funding

Clinical Research Special Project of Shanghai Municipal Health Commission 20254Y0118Interdisciplinary Program of Shanghai Jiaotong University YG2025QNB40National Natural Science Foundation of China 82270549National Natural Science Foundation of China 82372648National Natural Science Foundation of China 82470549National Natural Science Foundation of China 82570638Natural Science Foundation of Shanghai 22ZR1440500Natural Science Foundation of Shanghai 25ZR1402360
6 · The paper itself

Abstract

The E3 ubiquitin ligase tripartite motif 27 (TRIM27) is a negative regulator of NF-κB activation and the innate immune response, and TRIM27 deficiency significantly impairs dextran sulfate sodium (DSS)-induced colitis. The function of TRIM27 in intestinal epithelial cells (IECs), the mechanism by which TRIM27 inhibits the NF-κB pathway and its dysregulation in ulcerative colitis (UC) remain unclear. Here, it is report that epithelial TRIM27 functions as an anti-inflammatory factor that inhibited intestinal inflammation in IECs in vitro and in epithelial Trim27 knockout mice in vivo. Mechanistically, TRIM27 destabilized IKKα and TRAF6 via polyubiquitination of IKKα at the K569 site and TRAF6 at the K489 site. In response to TNF-α, IKKβ phosphorylated TRIM27 at S173 to decrease TRIM27 expression by impairing its binding to ubiquitin-specific protease 7 (USP7) and USP7-mediated TRIM27 deubiquitination. Notably, overexpression of TRIM27 enhanced the anti-inflammatory effect of infliximab (IFX) in IECs. TRIM27 is downregulated in inflamed colons from UC patients and is associated with the therapeutic effect of IFX. Overall, this study identifies epithelial TRIM27 as a bona fide negative modulator of intestinal inflammation and USP7/TRIM27-IKK as a new double negative feedback mechanism of the NF-κB pathway, which supports the use of TRIM27 replenishment as a potential therapeutic strategy for UC.

Indexed as

Colitis, UlcerativeDNA-Binding ProteinsI-kappa B KinaseInflammationIntestinal MucosaUbiquitin-Protein LigasesAnimalsDisease Models, AnimalEpithelial CellsHumansMiceMice, Inbred C57BLMice, KnockoutNF-kappa BNuclear ProteinsTripartite Motif ProteinsDNA-Binding ProteinsI-kappa B KinaseNF-kappa BNuclear ProteinsTRIM27 protein, humanTrim27 protein, mouseTripartite Motif ProteinsUbiquitin-Protein LigasesIKKintestinal inflammationTRIM27ulcerative colitisUSP7

Identifiers

PMID42017384
PMCPMC13335431

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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.