p53 and its isoforms in DNA double-stranded break repair.

Author: Yu-Xi ZHANG ¹ ; Wen-Ya PAN ¹ ; Jun CHEN ¹
Author Information

1. MOE Key Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, College of Life Sciences, Zhejiang University, Hangzhou 310058, China.
Publication Type:Journal Article
Keywords: p53; p53 isoform; DNA double-stranded break repair; Cell death
MeSH: Animals; DNA Breaks, Double-Stranded; DNA Repair; Humans; Mice; Protein Isoforms; physiology; Tumor Protein p73; physiology; Tumor Suppressor Protein p53; genetics; physiology
From: Journal of Zhejiang University. Science. B 2019;20(6):457-466
CountryChina
Language:English
Abstract: DNA double-stranded break (DSB) is one of the most catastrophic damages of genotoxic insult. Inappropriate repair of DNA DSBs results in the loss of genetic information, mutation, and the generation of harmful genomic rearrangements, which predisposes an organism to immunodeficiency, neurological damage, and cancer. The tumor repressor p53 plays a key role in DNA damage response, and has been found to be mutated in 50% of human cancer. p53, p63, and p73 are three members of the p53 gene family. Recent discoveries have shown that human p53 gene encodes at least 12 isoforms. Different p53 members and isoforms play various roles in orchestrating DNA damage response to maintain genomic integrity. This review briefly explores the functions of p53 and its isoforms in DNA DSB repair.