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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...
Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein.
Spreading of Chromatin Modifications02:25

Spreading of Chromatin Modifications

The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
The writer is an enzyme that can...
Histone Modification02:32

Histone Modification

The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone deacetylase,...

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Related Experiment Video

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A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia
09:52

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia

Published on: December 4, 2018

Acetylation controls Notch3 stability and function in T-cell leukemia.

R Palermo1, S Checquolo, A Giovenco

  • 1Department of Experimental Medicine, Sapienza University, Rome, Italy.

Oncogene
|November 29, 2011
PubMed
Summary
This summary is machine-generated.

Notch3 protein acetylation, regulated by p300 and HDAC1, controls its degradation. Inhibiting HDACs with HDAC inhibitors (HDACi) promotes Notch3 acetylation, reducing T-cell leukemia growth.

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Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Cancer Research

Background:

  • Post-translational modifications of Notch3 are crucial for T-cell leukemia but remain poorly understood.
  • Notch3 overexpression is implicated in T-cell malignancies, necessitating a deeper understanding of its regulation.

Purpose of the Study:

  • To investigate the role of Notch3 acetylation in T-cell leukemia.
  • To identify the enzymes regulating Notch3 acetylation and its functional consequences.

Main Methods:

  • Utilized HDAC inhibitors (HDACi) and a non-acetylatable Notch3 mutant (K/R 1692-1731).
  • Assessed Notch3 ubiquitination, degradation, protein expression, and transcriptional activity in vitro and in vivo.
  • Evaluated the effect of HDACi and Notch3 mutants on T-cell proliferation and leukemia growth in Notch3 transgenic mice.

Main Results:

  • Identified lysines 1692 and 1731 of Notch3 as targets for acetylation by p300 and deacetylation by HDAC1.
  • Demonstrated that Notch3 acetylation promotes its ubiquitination and proteasomal degradation.
  • Showed that HDACi treatment leads to Notch3 hyperacetylation, decreased Notch3 levels, and impaired downstream signaling.
  • Observed inhibition of Notch3-induced T-cell proliferation and leukemia growth by HDACi.

Conclusions:

  • Notch3 acetylation/deacetylation is a critical regulatory switch controlling Notch3 stability and signaling.
  • Targeting Notch3 acetylation with HDAC inhibitors offers a potential therapeutic strategy for Notch3-driven T-cell acute lymphoblastic leukemia.