Year: 2010
Type: preprint
Abstract: Mammalian cells are barraged with endogenous metabolic byproducts and environmental insults that can lead to nearly a million genomic lesions per cell per day. Networks of proteins that repair these lesions are essential for genome maintenance, and a compromise in these pathways propagates mutations that can cause aging and cancer. The p53 tumor suppressor plays a central role in repairing the effects of DNA damage, and has therefore earned the title of "guardian of the genome." In this issue of Genes & Development, Wilhelm and colleagues (pp. 549-560) demonstrate that p73-an older sibling of p53-inhibits pathways that resolve DNA double-strand breaks.
Source: Genes & Development
DOI: 10.1101/gad.1914210
Authors: Emma Vernersson-Lindahl, Alea A. Mills
Institution: Cold Spring Harbor Laboratory
Language: English
Topic: DNA Repair Mechanisms
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: diamond
OpenAlex ID: W1980608233