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Related Concept Videos

Notch Signaling Pathway03:14

Notch Signaling Pathway

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 until 1985...
Notch Signaling Pathway03:14

Notch Signaling Pathway

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 until 1985...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

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.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Intracellular Signaling Cascades01:24

Intracellular Signaling Cascades

Once a ligand binds to a receptor, the signal is transmitted through the membrane and into the cytoplasm. The continuation of a signal in this manner is called signal transduction. Signal transduction only occurs with cell-surface receptors, which cannot interact with most components of the cell, such as DNA. Only internal receptors can interact directly with DNA in the nucleus to initiate protein synthesis. When a ligand binds to its receptor, conformational changes occur that affect the...
Intracellular Signaling Cascades01:24

Intracellular Signaling Cascades

Once a ligand binds to a receptor, the signal is transmitted through the membrane and into the cytoplasm. The continuation of a signal in this manner is called signal transduction. Signal transduction only occurs with cell-surface receptors, which cannot interact with most components of the cell, such as DNA. Only internal receptors can interact directly with DNA in the nucleus to initiate protein synthesis. When a ligand binds to its receptor, conformational changes occur that affect the...
Catenins01:23

Catenins

Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
Catenins in Cell Junctions
Catenins bind to cell adhesion molecules such as cadherins and link them to different cytoskeletal proteins depending on the type of cell junction. At the adherens...

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Related Experiment Video

Updated: Jun 21, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

Notch signaling and CADASIL.

Sung-Chun Tang1, Jiann-Shing Jeng, Ming-Jen Lee

  • 1Stroke Center, National Taiwan University Hospital, Taiwan.

Acta Neurologica Taiwanica
|August 14, 2009
PubMed
Summary
This summary is machine-generated.

Cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy (CADASIL) is a genetic vascular disease. Understanding Notch3 gene mutations is key to diagnosing and treating this condition, which causes strokes and cognitive decline.

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Cell Aggregation Assays to Evaluate the Binding of the Drosophila Notch with Trans-Ligands and its Inhibition by Cis-Ligands
05:48

Cell Aggregation Assays to Evaluate the Binding of the Drosophila Notch with Trans-Ligands and its Inhibition by Cis-Ligands

Published on: January 2, 2018

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
09:08

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer

Published on: January 12, 2020

Related Experiment Videos

Last Updated: Jun 21, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

Cell Aggregation Assays to Evaluate the Binding of the Drosophila Notch with Trans-Ligands and its Inhibition by Cis-Ligands
05:48

Cell Aggregation Assays to Evaluate the Binding of the Drosophila Notch with Trans-Ligands and its Inhibition by Cis-Ligands

Published on: January 2, 2018

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
09:08

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer

Published on: January 12, 2020

Area of Science:

  • Neurology
  • Genetics
  • Vascular Biology

Background:

  • Notch signaling is crucial for vascular development and disease.
  • Mutations in the Notch3 gene cause cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy (CADASIL), a hereditary vascular disorder.
  • CADASIL is characterized by strokes and cognitive impairment, with increasing diagnoses but underestimated prevalence, particularly in Asia.

Purpose of the Study:

  • To review the clinical features of CADASIL.
  • To explore the potential pathogenesis of CADASIL.
  • To highlight the need for improved diagnostic accuracy and understanding of Notch3 mutation's role in brain damage.

Main Methods:

  • Literature review of clinical features and pathogenesis of CADASIL.
  • Analysis of the role of Notch3 gene mutations in vascular smooth muscle cell development and survival.
  • Examination of diagnostic advancements and their impact on CADASIL prevalence.

Main Results:

  • Notch3 is essential for vascular smooth muscle cell development and survival.
  • Pathogenic mechanisms of Notch3 mutations in CADASIL remain unclear.
  • Diagnostic improvements have increased CADASIL patient identification, yet prevalence is likely underestimated.

Conclusions:

  • Further research is needed to elucidate the pathogenic mechanisms of Notch3 mutations in CADASIL.
  • Continued efforts are essential to enhance diagnostic accuracy for CADASIL.
  • Defining the precise role of Notch3 mutations in CADASIL-related brain damage and clinical manifestations is critical.