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Related Concept Videos

Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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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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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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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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Inflammatory Bowel Disease II: Ulcerative Colitis01:20

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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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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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Related Experiment Video

Updated: May 7, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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Ubiquitin-Modifying Enzymes as Cell-Fate Regulators in Intestinal Inflammation.

Chenchen Qian1,2, Fangmin Ning1, Yong Xu1

  • 1School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang 311121, China.

International Journal of Biological Sciences
|May 6, 2026
PubMed
Summary
This summary is machine-generated.

Ubiquitin-modifying enzymes (UMEs) are crucial for maintaining intestinal health by controlling cell fate. Dysregulation of UMEs is linked to inflammatory bowel disease (IBD), suggesting their potential as therapeutic targets.

Keywords:
cell fateinflammatory bowel diseasepost-translational modificationsubiquitin-modifying enzymes

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Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Immunology

Background:

  • Inflammatory bowel disease (IBD), encompassing ulcerative colitis (UC) and Crohn's disease (CD), is a chronic gastrointestinal inflammatory condition.
  • Intestinal homeostasis depends on precise cell fate regulation in the epithelium and immune system.
  • Ubiquitin-modifying enzymes (UMEs) are key regulators of protein stability, activity, and localization, influencing these cellular processes.

Purpose of the Study:

  • To review the critical roles of UMEs in cell fate determination within the intestine.
  • To examine the impact of UMEs on intestinal barrier function and immune responses.
  • To discuss the involvement of UMEs in IBD pathogenesis and their potential as therapeutic targets.

Main Methods:

  • Systematic review of current literature on UMEs and intestinal homeostasis.
  • Analysis of the role of UMEs in regulating intestinal epithelial and immune cell fate.
  • Exploration of UME dysregulation in IBD and potential therapeutic strategies.

Main Results:

  • UMEs are essential for controlling cell fate decisions impacting intestinal barrier integrity and immune responses.
  • Specific UMEs are pathologically dysregulated in IBD, indicating their involvement in disease development.
  • UMEs show promise as diagnostic biomarkers and therapeutic targets for IBD management.

Conclusions:

  • UMEs play a fundamental role in ubiquitin-mediated regulation of intestinal cell fate.
  • Targeting UMEs offers novel therapeutic avenues for managing IBD and preventing colitis-associated cancer (CAC).
  • Emerging strategies like small-molecule inhibitors and PROTAC technology present new clinical applications for UME-targeted therapies.