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Related Concept Videos

Inflammatory Bowel Disease II: Crohn's Disease01:30

Inflammatory Bowel Disease II: Crohn's Disease

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Introduction
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Related Experiment Video

Updated: Dec 15, 2025

Evaluating Therapeutic Interventions in the SHIP-deficient Mouse Model of Crohn Disease-like Ileitis and Fibrosis
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RIPK2 NODs to XIAP and IBD.

Yusuf Topal1, Mads Gyrd-Hansen1

  • 1Ludwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus Research Building, Oxford, OX3 7DQ, UK.

Seminars in Cell & Developmental Biology
|July 8, 2020
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Summary

Receptor-interacting protein kinase 2 (RIPK2) is crucial for intestinal immunity and inflammation. Targeting the RIPK2-XIAP interaction offers a new therapeutic strategy for immune-related disorders.

Keywords:
Blau syndromeInflammatory bowel diseaseNOD1NOD2RIPK2Therapeutic targetUbiquitin signallingXIAP

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Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Receptor-interacting protein kinases (RIPKs) regulate inflammatory signaling and cell death.
  • RIPK2 is essential for bacterial-sensing pattern recognition receptors NOD1/2-mediated signaling.
  • NOD1/2 pathways are critical for intestinal immunity and inflammation.

Purpose of the Study:

  • To discuss the mechanistic function of RIPK2 in immune signaling.
  • To highlight the clinical relevance of RIPK2 in immune-related disorders.
  • To review efforts targeting RIPK2 for inflammatory bowel disease.

Main Methods:

  • Review of recent advances in understanding RIPK2 signaling.
  • Analysis of the role of XIAP in RIPK2 ubiquitination.
  • Discussion of druggable protein-protein interactions involving RIPK2 and XIAP.

Main Results:

  • RIPK2 mediates NOD1/2 signaling through ubiquitination.
  • XIAP and other ligases generate non-degradative ubiquitin chains on RIPK2.
  • The RIPK2-XIAP interaction is a potential therapeutic target.

Conclusions:

  • RIPK2 plays a central role in innate immune responses.
  • Targeting RIPK2 offers a promising therapeutic avenue for inflammatory conditions.
  • Modulating NOD1/2-dependent immune responses via RIPK2 is under investigation for inflammatory bowel disease.