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Related Experiment Video

Updated: Jan 19, 2026

In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones
11:36

In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones

Published on: July 25, 2019

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USP7 Deubiquitinates and Stabilizes SIRT1.

Nan Song1, Cheng Cao1, Shanshan Tian1

  • 12011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics, Department of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, China.

Anatomical Record (Hoboken, N.J. : 2007)
|September 11, 2019
PubMed
Summary

The ubiquitin-specific protease USP7 stabilizes silent information regulator 1 (SIRT1) by removing polyubiquitin chains. This discovery reveals a new mechanism controlling SIRT1 protein levels in cells.

Keywords:
SIRT1USP7deubiquitination

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Nuclear Stability: Valley of Stability and Magic Numbers
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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Silent Information Regulator 1 (SIRT1) is a NAD+-dependent protein deacetylase involved in numerous cellular pathways and diseases.
  • The regulation of SIRT1 protein abundance remains largely uncharacterized.

Purpose of the Study:

  • To investigate the regulatory mechanisms governing SIRT1 protein levels.
  • To identify proteins interacting with SIRT1 and their functional roles.

Main Methods:

  • Mass spectrometry was employed to analyze SIRT1-containing protein complexes.
  • Cellular treatments with a USP7 enzymatic inhibitor were performed.
  • Polyubiquitination levels of SIRT1 were assessed.

Main Results:

  • SIRT1 was found to physically associate with USP7.
  • USP7 was identified as an enzyme that cleaves K48-linked polyubiquitin chains from SIRT1.
  • Inhibition of USP7 activity resulted in reduced SIRT1 expression and increased SIRT1 polyubiquitination.

Conclusions:

  • USP7 is a critical regulator of SIRT1 stability.
  • USP7 promotes SIRT1 stabilization by deubiquitination, providing a novel pathway for maintaining SIRT1 abundance.