P53 and Sirt1: Routes of metabolism and genome stability

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P53 and Sirt1: Routes of metabolism and genome stability

Authors
  • Bellusci, Giovanna
  • Ciccone, Sarah
  • Marc Diederich
  • Gonfloni, Stefania
  • Iannizzotto, Valentina
  • Maiani, Emiliano
Type
Published Article
Journal
Biochemical Pharmacology
Publisher
Elsevier
Publication Date
Nov 24, 2014
Volume
92
Issue
1
Pages
156–156
Identifiers
DOI: 10.1016/j.bcp.2014.08.034
Source
LBMCC
Keywords
License
Green

Abstract

The tumor suppressor p53 is a transcription factor that regulates key processes. But, the outcomes of the p53 response go beyond its role as a nuclear transcription factor. Sirtuin (SIRT1) regulates p53 functions as transcription factor. At the same time, SIRT1 protects the genome under stress conditions. The link between p53 and SIRT1 responses is unique. Both regulate metabolism, stress signaling, cell survival, cell cycle control and genome stability. Recent studies have proposed cancer as a metabolic disease. This is due to the switch from aerobic to anaerobic metabolism during tumor development. Yet, the complex molecular circuits (in and out of the nucleus) of tumor progression remain elusive. In this review, we will focus on the interplay between p53 and SIRT1. We will discuss their roles as nodes for possible therapeutic intervention.

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