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Related Concept Videos

DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Abnormal Proliferation02:23

Abnormal Proliferation

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 daughter...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

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Related Experiment Video

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Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method
09:32

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EDD induces cell cycle arrest by increasing p53 levels.

Veronique A J Smits1

  • 1Unidad de Investigación, Hospital Universitario de Canarias, Instituto de Tecnologias Biomedicas, Tenerife, Spain. vsmits@ull.es

Cell Cycle (Georgetown, Tex.)
|March 1, 2012
PubMed
Summary

EDD (also known as UBR5/hHyd) is a novel regulator of p53, a key protein for genome stability. EDD downregulation increases p53 levels, triggering cell cycle arrest and senescence.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The p53 protein is crucial for maintaining genomic stability and preventing tumor formation.
  • Tight regulation of p53 is essential for its tumor suppressor functions.
  • Identifying novel regulators of p53 is key to understanding its complex roles in cellular processes.

Purpose of the Study:

  • To identify novel regulators of the p53 protein.
  • To investigate the role of EDD/UBR5/hHyd (EDD) in p53 regulation.
  • To elucidate the functional consequences of EDD downregulation on cellular processes.

Main Methods:

  • Depletion of EDD using knockdown techniques in both transformed and untransformed cells.
  • Analysis of p53 and p21 protein and mRNA levels.

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Yeast As a Chassis for Developing Functional Assays to Study Human P53

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Last Updated: May 24, 2026

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method
09:32

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Published on: September 10, 2017

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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  • Assessment of p53 protein stability.
  • Induction of senescence in fibroblasts.
  • Cell cycle progression analysis using flow cytometry.

    • Main Results:

    • Downregulation of EDD leads to elevated p53 protein levels without affecting p53 mRNA or protein stability.
    • Increased p53 levels upon EDD depletion result in elevated p21 levels, a known p53 target.
    • EDD downregulation triggers a senescent phenotype in fibroblasts.
    • Increased p53 levels upon EDD depletion cause G1 cell cycle arrest, which is rescued by simultaneous depletion of p53.

    Conclusions:

    • EDD is identified as a novel regulator of p53 protein levels.
    • EDD plays a significant role in controlling p53-mediated cellular responses, including cell cycle arrest and senescence.
    • Targeting EDD may offer a new strategy for cancer therapy by modulating p53 activity.