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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...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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...
Differentiation of Common Myeloid Progenitor Cells01:15

Differentiation of Common Myeloid Progenitor Cells

Common myeloid progenitors (CMPs) are oligopotent cells that can differentiate into granulocytes and macrophages. Granulocytes and macrophages are essential for protecting the body against bacterial, viral, or fungal infections. They migrate from the bone marrow into the circulating blood to reach specific tissue sites where they differentiate and help in immune surveillance. However, they survive only for a few days and must be continuously made available to the organism to maintain a robust...

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Related Experiment Video

Updated: Jul 9, 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 in leukemia.

Jon C Aster1, Warren S Pear, Stephen C Blacklow

  • 1Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. jaster@partners.org

Annual Review of Pathology
|November 28, 2007
PubMed
Summary
This summary is machine-generated.

Gain-of-function mutations in Notch1 receptors are frequent in T cell acute lymphoblastic leukemia/lymphoma. Understanding these mutations offers insights into Notch1 signaling and potential new cancer therapies.

More Related Videos

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: Jul 9, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

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:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Notch1 receptor signaling is crucial in cellular development and differentiation.
  • Aberrant Notch1 signaling is implicated in various human cancers, particularly T cell acute lymphoblastic leukemia/lymphoma (T-ALL).
  • Gain-of-function mutations in Notch1 are increasingly recognized as a common driver in T-ALL pathogenesis.

Purpose of the Study:

  • To review the current understanding of Notch1 signaling in normal physiology and T-ALL.
  • To elucidate the impact of gain-of-function mutations on Notch1 pathway activity in T-ALL.
  • To explore the therapeutic potential of targeting Notch1 signaling in T-ALL.

Main Methods:

  • Literature review of recent studies on Notch1 mutations in T-ALL.
  • Analysis of data linking Notch1 signaling pathways to cancer development.
  • Synthesis of information on targeted therapy strategies.

Main Results:

  • Gain-of-function mutations in Notch1 are a prevalent feature of human T-ALL.
  • These mutations lead to dysregulated Notch1 signaling, promoting leukemogenesis.
  • Insights from these mutations highlight Notch1 as a critical target for therapeutic intervention.

Conclusions:

  • Notch1 receptor mutations are key drivers in T-ALL.
  • Understanding Notch1 signaling provides a foundation for developing novel targeted therapies.
  • Targeting Notch1 offers a promising strategy for treating this aggressive leukemia.