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Abnormal Proliferation

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...

Covalently Linked Protein Regulators

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.

DNA Damage can Stall the Cell Cycle

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 Cycle

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Negative Regulator Molecules

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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.

Separation of Sister Chromatids

Separation of Sister Chromatids

At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
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Related Experiment Video

Updated: Jun 25, 2026

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

p53 ubiquitination by Mdm2: a never ending tail?

Amanda S Coutts¹, Cassandra J Adams, Nicholas B La Thangue

¹Medical Sciences Division, Department of Clinical Pharmacology, University of Oxford, Oxford OX3 7DQ, UK.

|February 17, 2009

Summary

The tumor suppressor p53 is crucial for preventing cancer. Its regulation by Mdm2 involves ubiquitination, which impacts both p53 protein levels and activity, directing cellular responses to stress.

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Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model

Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model

Published on: April 17, 2026

Area of Science:

Molecular Biology
Cancer Research
Cellular Biology

Background:

The tumor suppressor protein p53 is vital for preventing human cancer.
p53 levels are tightly regulated in normal cells, with Mdm2 mediating its degradation.
Ubiquitination of p53 was traditionally viewed as a mechanism for degradation.

Purpose of the Study:

To review the current understanding of p53 ubiquitination by Mdm2.
To highlight how ubiquitination influences p53 activity beyond just protein stability.
To explore the interplay between p53 levels, ubiquitination, and other post-translational modifications.

Main Methods:

Literature review of recent studies on p53-Mdm2 interactions.
Analysis of research on p53 ubiquitination and its functional consequences.
Synthesis of data on post-translational modifications affecting p53.

Main Results:

Ubiquitination by Mdm2 can modulate p53 activity, not solely its degradation.
The balance of p53 protein levels and post-translational modifications dictates cellular responses.
Mdm2-mediated ubiquitination is a complex regulatory mechanism for p53.

Conclusions:

Understanding p53 ubiquitination is key to comprehending cancer suppression.
The regulation of p53 involves a dynamic balance of stability and activity.
Future research should focus on the intricate post-translational modifications of p53.