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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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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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Regulation of Angiogenesis and Blood Supply01:24

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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...
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The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
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Related Experiment Video

Updated: Apr 28, 2026

The Power of Simplicity: Sea Urchin Embryos as in Vivo Developmental Models for Studying Complex Cell-to-cell Signaling Network Interactions
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A Snail1/Notch1 signalling axis controls embryonic vascular development.

Zhao-Qiu Wu1, R Grant Rowe2, Kim-Chew Lim3

  • 11] Division of Molecular Medicine and Genetics, Department of Internal Medicine, Ann Arbor, Michigan 48109, USA [2] Life Sciences Institute, Ann Arbor, Michigan 48109, USA.

Nature Communications
|June 5, 2014
PubMed
Summary
This summary is machine-generated.

The transcriptional repressor Snail1 regulates vascular development by controlling Notch1-Delta-like 4 (Dll4) signaling. Snail1 deficiency disrupts vessel remodeling and arterial-venous specification in developing embryos.

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Area of Science:

  • Vascular Biology
  • Developmental Biology
  • Molecular Signaling

Background:

  • Notch1-Delta-like 4 (Dll4) signaling is crucial for vascular development, regulating endothelial cell targets involved in vessel remodeling and arterial-venous specification.
  • The specific molecular mechanisms and effectors that modulate Notch signaling during embryonic vascular development are not fully understood.

Purpose of the Study:

  • To identify molecular regulators of Notch signaling during vascular development.
  • To investigate the role of the transcriptional repressor Snail1 in Notch signaling and its impact on embryonic vascular development.

Main Methods:

  • Utilized endothelial cell (EC)-specific Snail1 loss-of-function conditional knockout mouse models.
  • Analyzed embryonic lethality, vessel wall remodeling defects, mural cell investment, and arterial-venous specification.
  • Investigated Notch1 signaling and Dll4 expression levels.
  • Employed in vivo gamma-secretase inhibition to assess the role of Notch signaling.

Main Results:

  • EC-specific Snail1 loss-of-function resulted in embryonic lethality with severe defects in vessel wall remodeling, mural cell investment, and arterial-venous specification.
  • Snail1-deficient embryos exhibited upregulated Notch1 signaling and Dll4 expression.
  • Dll4 was identified as a direct transcriptional target repressed by Snail1.
  • Inhibition of gamma-secretase partially reversed the upregulated Notch1 signaling and Dll4 expression in knockout embryos.

Conclusions:

  • The transcriptional repressor Snail1 acts as a key regulator of vascular development.
  • Snail1 modulates vascular development through a Snail1-Dll4/Notch1 signaling axis.
  • This axis is critical for embryonic vascular remodeling and arterial-venous specification.