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Related Concept Videos

Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

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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.
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...
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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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Cell-surface Signaling01:21

Cell-surface Signaling

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Hormones—or any molecule that binds to a receptor, known as a ligand—that are lipid-insoluble (water-soluble) are not able to diffuse across the cell membrane. In order to be able to affect a cell without entering it, these hormones bind to receptors on the cell membrane. When a first messenger, a hormone, binds to a receptor, a signal cascade is set off, causing second messengers, proteins inside the cell, to become activated, resulting in downstream effects.
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Decreasing Function01:27

Decreasing Function

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A decreasing function describes a relationship where the output consistently declines as the input increases. This means that for any two input values, if one is greater than the other, the corresponding output is smaller. Mathematically, a function f is decreasing on an interval I if for every x1 < x2​ in I, f (x1) > f (x2). This type of behavior is visually identified on a graph that slopes downward from left to right.The nature of a function can be analyzed by calculating...
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What is Cell Signaling?02:03

What is Cell Signaling?

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Despite the protective membrane that separates a cell from the environment, cells need the ability to detect and respond to environmental changes. Additionally, cells often need to communicate with one another. Unicellular and multicellular organisms use a variety of cell signaling mechanisms to communicate to respond to the environment.
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The Mitotic Spindle02:27

The Mitotic Spindle

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The mitotic spindle—or spindle apparatus—is a eukaryotic, cytoskeletal structure made up of long protein fibers called microtubules. Formed during cell division, the spindle separates sister chromatids and moves them to opposite ends of a parental cell, where the now individual chromosomes are distributed to two daughter cell nuclei.
The bipolar configuration of the mitotic spindle facilitates chromosomal segregation, preparing the cell for division. One mechanism that ensures...
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Related Experiment Video

Updated: Feb 4, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
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Impaired Notch Signaling Leads to a Decrease in p53 Activity and Mitotic Catastrophe in Aged Muscle Stem Cells.

Ling Liu1, Gregory W Charville2, Tom H Cheung3

  • 1Paul F. Glenn Center for the Biology of Aging and Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.

Cell Stem Cell
|September 25, 2018
PubMed
Summary
This summary is machine-generated.

Aging impairs muscle stem cell regeneration due to cell death. Activating the Notch-p53 pathway in muscle stem cells (MuSCs) can restore their function and promote tissue repair in older animals.

Keywords:
Notchagingmitotic catastrophemuscle regenerationmuscle stem cellsp53satellite cellsstem cells

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Related Experiment Videos

Last Updated: Feb 4, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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Area of Science:

  • Aging and regenerative medicine
  • Stem cell biology
  • Molecular signaling

Background:

  • Tissue regenerative potential declines with age, linked to impaired stem cell function.
  • Therapeutic strategies to modulate aging stem cells are limited.
  • Skeletal muscle stem cells (MuSCs) are crucial for muscle repair.

Purpose of the Study:

  • To identify causes of impaired stem cell proliferation in aged animals.
  • To investigate the role of the Notch-p53 signaling axis in MuSC function during aging.
  • To explore therapeutic potential of modulating this pathway for age-related muscle degeneration.

Main Methods:

  • Utilized aged animal models and skeletal muscle stem cells (MuSCs).
  • Investigated cell death mechanisms, specifically mitotic catastrophe.
  • Analyzed Notch signaling, p53 activation, and Mdm2 expression via Hey transcription factors.
  • Assessed the effect of pharmacologic p53 activation in vivo.

Main Results:

  • Identified mitotic catastrophe as a cause of reduced MuSC expansion in aged animals.
  • Found deficiency in microenvironmental Notch activators contributes to impaired MuSC function.
  • Discovered a functional Notch-p53 signaling axis (Notch → Hey → Mdm2 inhibition → p53 activation) essential for MuSC survival.
  • Demonstrated that pharmacologic p53 activation promotes expansion of aged MuSCs in vivo.

Conclusions:

  • A Notch-p53 signaling axis is critical for MuSC survival and function during muscle regeneration.
  • This pathway is dysregulated in aged animals, contributing to reduced muscle regenerative capacity.
  • Targeting the Notch-p53 axis offers a potential therapeutic strategy to enhance stem cell function and combat age-related tissue degeneration.