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Related Concept Videos

Notch Signaling Pathway03:14

Notch Signaling Pathway

4.5K
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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Notch Signaling Pathway03:14

Notch Signaling Pathway

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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...
1.7K
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

8.6K
The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
8.6K
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

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Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
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Abnormal Proliferation02:23

Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Related Experiment Video

Updated: Apr 21, 2026

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
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T-ALL pathogenesis requires a NOTCH1-driven MYC enhancer

    Cancer Discovery
    |November 5, 2014
    PubMed
    Summary

    A MYC enhancer bound by NOTCH1 is crucial for T-cell development and T-cell acute lymphoblastic leukemia (T-ALL) caused by NOTCH1.

    Area of Science:

    • Immunology and Cancer Biology

    Background:

    • The NOTCH1 signaling pathway is vital in T-cell development.
    • Dysregulation of NOTCH1 signaling is implicated in T-cell acute lymphoblastic leukemia (T-ALL).

    Purpose of the Study:

    • To investigate the role of a specific MYC enhancer in NOTCH1-mediated T-cell development and T-ALL.

    Main Methods:

    • Utilized genetic manipulation and molecular assays to study enhancer function.
    • Analyzed T-cell development and leukemia progression in relevant models.

    Main Results:

    • Identified a MYC enhancer that directly binds to NOTCH1.
    • Demonstrated that this NOTCH1-bound MYC enhancer is essential for normal T-cell development.
    • Showed the enhancer's necessity in NOTCH1-driven T-ALL pathogenesis.

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    Conclusions:

    • A NOTCH1-bound MYC enhancer plays a critical regulatory role in T-cell differentiation.
    • This enhancer is a key mediator in the development of T-cell acute lymphoblastic leukemia driven by NOTCH1.