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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 27, 2026

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

Usp7 protects genomic stability by regulating Bub3.

Serena Giovinazzi¹, Pietro Sirleto, Vasilisa Aksenova

¹Department of Anatomy and Cell Biology, University of Florida College of Medicine, Gainesville, FL; University of Florida Health Cancer Center, Gainesville, FL.

|July 9, 2014

Summary

Ubiquitin Specific Processing Protease-7 (USP7) regulates genomic stability by controlling the spindle assembly checkpoint component Bub3. USP7 inhibition causes mitotic abnormalities, highlighting its potential in cancer therapy.

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Area of Science:

Cell Biology
Molecular Biology
Genetics

Background:

Ubiquitin Specific Processing Protease-7 (USP7) is a deubiquitinase regulating cellular processes.
USP7 deregulation is linked to cancer, making USP7 inhibition a potential anti-cancer strategy.

Purpose of the Study:

To investigate the novel function of USP7 in maintaining genomic stability.
To identify USP7 substrates and related cellular activities for potential clinical applications.

Main Methods:

USP7 depletion and inhibition using small molecule inhibitors.
Analysis of mitotic progression, chromosomal abnormalities, and protein levels (e.g., cyclin B, Bub3).
In silico analysis of USP7 levels and genomic instability across NCI-60 cell lines.

Main Results:

USP7 depletion leads to prolonged mitosis, micronuclei accumulation, lagging chromosomes, and karyotype instability.
USP7 inhibition stabilizes cyclin B and induces mitotic abnormalities.
USP7 interacts with and deubiquitinates Bub3, a spindle assembly checkpoint component, leading to decreased Bub3 levels.
Lower USP7 levels correlate with genomic instability in NCI-60 cell lines.

Conclusions:

USP7 plays a novel and critical role in regulating the spindle assembly checkpoint (SAC) component Bub3.
USP7 is essential for maintaining genomic stability.
USP7 inhibition presents a promising avenue for anti-cancer therapeutic strategies.