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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...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...

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Related Experiment Video

Updated: May 25, 2026

Real-time Bioluminescence Imaging of Notch Signaling Dynamics during Murine Neurogenesis
10:25

Real-time Bioluminescence Imaging of Notch Signaling Dynamics during Murine Neurogenesis

Published on: December 12, 2019

Pten coordinates retinal neurogenesis by regulating Notch signalling.

Hong Seok Jo1, Kyung Hwa Kang, Cheol O Joe

  • 1Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.

The EMBO Journal
|January 20, 2012
PubMed
Summary

Phosphatase tensin homologue (Pten) is crucial for maintaining neural progenitor cells (NPCs) in the mouse retina. Its absence causes premature depletion of NPCs, impacting retinal development.

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Cell Signaling

Background:

  • Nervous system development relies on a balance between neural progenitor cell (NPC) proliferation and neuronal differentiation.
  • Intracellular signaling pathways critically regulate this balance, influencing the final size and composition of nervous tissues.

Purpose of the Study:

  • To investigate the role of phosphatase tensin homologue (Pten) in regulating neural progenitor cell (NPC) maintenance within the mouse retina.
  • To elucidate the molecular mechanisms by which Pten controls the balance between NPC proliferation and neuronal differentiation.

Main Methods:

  • Utilized genetically modified mouse models lacking the Pten gene in retinal progenitor cells (RPCs).
  • Analyzed neurogenesis timing and NPC population dynamics in Pten-deficient and wild-type retinas.
  • Investigated the interaction between Pten, PI3K-Akt signaling, and Notch intracellular domain (NICD) signaling pathways.

Main Results:

  • Pten deficiency in mouse RPCs led to accelerated neurogenesis and premature depletion of the NPC pool.
  • Pten-deficient RPCs exhibited impaired formation of the Notch intracellular domain (NICD) transcription activator complex.
  • This disruption in NICD complex formation hindered the maintenance of RPCs.

Conclusions:

  • Pten is essential for maintaining the neural progenitor cell population in the developing mouse retina.
  • Pten negatively regulates phosphoinosite 3-kinase (PI3K)-Akt signaling, thereby supporting Notch-driven RPC maintenance.
  • Pten plays a critical role in retinal neurogenesis by balancing pro-neurogenic signaling with progenitor cell maintenance.