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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...
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...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

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 are of three kinds RI, RII, and RIII. The RI...
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...
Bone Formation by Endochondral Ossification01:24

Bone Formation by Endochondral Ossification

Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...

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Related Experiment Video

Updated: Jun 14, 2026

Protein Isolation from the Developing Embryonic Mouse Heart Valve Region
06:55

Protein Isolation from the Developing Embryonic Mouse Heart Valve Region

Published on: September 23, 2014

Notch1 represses osteogenic pathways in aortic valve cells.

Vishal Nigam1, Deepak Srivastava

  • 1Gladstone Institute of Cardiovascular Disease and Departments of Pediatrics, University of California, San Francisco, CA 94158, USA. vnigam@ucsd.edu

Journal of Molecular and Cellular Cardiology
|August 22, 2009
PubMed
Summary

Notch1 signaling normally prevents aortic valve calcification. Its inhibition promotes osteoblast-like gene expression and calcification, mediated by bone morphogenic protein 2 (Bmp2).

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Stimulation of Notch Signaling in Mouse Osteoclast Precursors
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Stimulation of Notch Signaling in Mouse Osteoclast Precursors

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Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
05:47

Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro

Published on: May 10, 2021

Related Experiment Videos

Last Updated: Jun 14, 2026

Protein Isolation from the Developing Embryonic Mouse Heart Valve Region
06:55

Protein Isolation from the Developing Embryonic Mouse Heart Valve Region

Published on: September 23, 2014

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
05:47

Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro

Published on: May 10, 2021

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Genetics of Valvular Heart Disease

Background:

  • Calcific aortic stenosis is a prevalent cause of adult heart disease.
  • Molecular mechanisms underlying aortic valve calcification remain poorly understood.
  • NOTCH1 mutations are linked to bicuspid aortic valve and calcification.

Purpose of the Study:

  • To elucidate the mechanism by which NOTCH1 represses aortic valve calcification.
  • To investigate the role of Notch signaling in aortic valve interstitial cells (AVICs).

Main Methods:

  • Utilized heterozygous Notch1-null mice to assess in vivo calcification.
  • Inhibited Notch signaling in cultured sheep AVICs to evaluate calcification and gene expression.
  • Examined the effect of bone morphogenic protein 2 (Bmp2) on Notch inhibition-induced calcification.

Main Results:

  • Notch1-null mice exhibited significantly increased aortic valve calcification.
  • Notch inhibition in AVICs led to a fivefold increase in calcification and osteoblast-like gene expression.
  • Notch1 was found to repress Bmp2 expression in aortic valve cells.
  • Bmp2 knockdown abrogated calcification induced by Notch inhibition in AVICs.

Conclusions:

  • Notch1 signaling plays a crucial role in repressing osteoblast-like calcification pathways in aortic valves.
  • Bone morphogenic protein 2 (Bmp2) is a key mediator of Notch-dependent aortic valve calcification.