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Related Concept Videos

Notch Signaling Pathway03:14

Notch Signaling Pathway

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The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
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Notch Signaling Pathway03:14

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Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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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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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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Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

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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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TGF - β Signaling Pathway01:16

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Related Experiment Video

Updated: May 3, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
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Increased Notch pathway activation in Behçet's disease.

Jian Qi1, Yan Yang, Shengping Hou

  • 1First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, and Chongqing Eye Institute, Chongqing 400016, China. peizengycmu@126.com.

Rheumatology (Oxford, England)
|January 22, 2014
PubMed
Summary

The Notch pathway is activated in Behçet

Keywords:
Behçet’sT cellsautoinflammatory conditionscell receptor–ligand interactioncytokines and inflammatory mediatorsinflammationlymphocytesmicroRNAmolecular biologyophthalmicsignalling and activation

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Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Behçet's disease (BD) is a complex inflammatory condition with poorly understood etiology.
  • The Notch signaling pathway plays a crucial role in regulating immune cell function and differentiation.

Purpose of the Study:

  • To investigate the involvement of the Notch pathway in the pathogenesis of Behçet's disease.
  • To explore the relationship between Notch pathway activation and T helper 17 (Th17) cell responses in BD.

Main Methods:

  • Gene expression analysis (real-time PCR) of Notch pathway components (Notch 1-4, Jagged-1, DLL-1, DLL-4, Hes-1).
  • Flow cytometry to quantify T helper cell subsets expressing IFN-γ and IL-17.
  • ELISA for cytokine production and assessment of Notch intracellular domain (NICD) and phosphorylated STAT3 (p-STAT3).
  • Pharmacological inhibition of Notch signaling using DAPT and modulation of miR-23b levels.

Main Results:

  • Active Behçet's disease patients exhibit heightened Notch pathway activation correlating with increased Th17 responses.
  • Notch pathway blockade significantly reduced Th17 responses and STAT3 phosphorylation.
  • miR-23b expression was diminished in CD4(+) T cells of BD patients; its restoration decreased NICD expression and IL-17/IFN-γ production.

Conclusions:

  • Aberrant Notch pathway activation appears to contribute to Behçet's disease pathogenesis.
  • Reduced miR-23b levels may drive Notch pathway overactivation in BD.
  • Targeting the Notch pathway presents a potential therapeutic strategy for Behçet's disease.