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Related Concept Videos

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...
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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.
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

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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.
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Related Experiment Video

Updated: Jul 11, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

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

Published on: August 4, 2019

MAGED2: a novel p53-dissociator.

Chris Papageorgio1, Rainer Brachmann, Jue Zeng

  • 1Hematology and Medical Oncology, Ellis Fischel Cancer Center, University of Missouri-Columbia, Columbia, MO 65203, USA. papageorgioc@health.missouri.edu

International Journal of Oncology
|October 4, 2007
PubMed
Summary
This summary is machine-generated.

Researchers identified MAGED2 as a novel protein that negatively regulates wild-type p53 activity. MAGED2 interacts with p53, affecting its function in cancer cells and tissues.

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Yeast As a Chassis for Developing Functional Assays to Study Human P53
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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Protein Interactions

Background:

  • The tumor suppressor protein p53 is a critical transcription factor frequently mutated in human cancers.
  • Wild-type p53 (wt p53) is activated by post-transcriptional modifications upon DNA damage, inducing apoptosis or cell cycle arrest.

Purpose of the Study:

  • To identify novel regulators of wild-type p53 activity.
  • To investigate the role of MAGED2 in modulating p53 function.

Main Methods:

  • Yeast p53-dissociator assay to identify potential regulators.
  • Co-immunoprecipitation and reporter gene assays in human cultured cells.
  • Analysis of p53 and MAGED2 co-expression in human cancer tissue microarrays.

Main Results:

  • MAGED2 was identified as a potential negative regulator of wt p53.
  • MAGED2 physically interacts with p53 and modifies its activity in human cells.
  • Co-expression of p53 and MAGED2 was observed in the nucleus and cytoplasm of 2,682 human cancer specimens.

Conclusions:

  • MAGED2 acts as a novel p53-dissociator, negatively regulating wt p53 activity.
  • The interaction between MAGED2 and p53 has implications for cancer biology.
  • MAGED2 represents a potential target for cancer therapy.