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Related Concept Videos

Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

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Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal...
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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
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Inflammatory Bowel Disease III: Crohn's Disease01:25

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Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
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Inflammatory Bowel Disease I: Ulcerative Colitis01:27

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Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
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Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
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Related Experiment Video

Updated: Apr 23, 2026

An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
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Epithelial TRIM27 Inhibits Intestinal Inflammation in Ulcerative Colitis by the USP7/TRIM27-IKK Double

Weimin Xu1,2, Zhebin Hua1,2, Zhujiang Dai1,2

  • 1Department of Colorectal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|April 22, 2026
PubMed
Summary

Epithelial TRIM27 acts as an anti-inflammatory factor, reducing intestinal inflammation by destabilizing key proteins in the NF-κB pathway. This finding suggests TRIM27 replenishment may be a novel therapeutic strategy for ulcerative colitis.

Keywords:
IKKTRIM27USP7intestinal inflammationulcerative colitis

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Area of Science:

  • Immunology
  • Molecular Biology
  • Gastroenterology

Background:

  • Tripartite motif 27 (TRIM27) is an E3 ubiquitin ligase that negatively regulates NF-κB activation and innate immunity.
  • TRIM27 deficiency exacerbates dextran sulfate sodium (DSS)-induced colitis, but its role in intestinal epithelial cells (IECs) and ulcerative colitis (UC) is unclear.

Purpose of the Study:

  • To elucidate the function and mechanism of TRIM27 in intestinal epithelial cells (IECs) regarding inflammation.
  • To investigate the role of TRIM27 in the NF-κB pathway and its dysregulation in ulcerative colitis (UC).
  • To assess the therapeutic potential of TRIM27 in inflammatory bowel disease.

Main Methods:

  • In vitro studies using IECs and in vivo studies using epithelial Trim27 knockout mice.
  • Investigated TRIM27's mechanism by analyzing polyubiquitination of IKKα and TRAF6.
  • Examined the effect of TNF-α on TRIM27 phosphorylation and its interaction with USP7.
  • Assessed TRIM27 expression in UC patient samples and its association with infliximab (IFX) therapy.

Main Results:

  • Epithelial TRIM27 demonstrated anti-inflammatory effects in both in vitro and in vivo models.
  • TRIM27 destabilizes IKKα and TRAF6 through specific polyubiquitination sites (K569 and K489, respectively).
  • TNF-α-induced phosphorylation of TRIM27 at S173 impairs its deubiquitination by USP7, reducing TRIM27 expression.
  • TRIM27 overexpression enhanced infliximab's anti-inflammatory effect, and TRIM27 was downregulated in UC patients.

Conclusions:

  • Epithelial TRIM27 is a critical negative regulator of intestinal inflammation.
  • A novel USP7/TRIM27-IKK double negative feedback loop in the NF-κB pathway was identified.
  • TRIM27 replenishment represents a potential therapeutic strategy for ulcerative colitis.