Induction of p57KIP2 expression by p73β

Éva Bálint, Andrew C. Phillips, Serguei Kozlov, Colin L. Stewart, Karen H. Vousden

Research output: Contribution to journalArticle

85 Citations (Scopus)

Abstract

The p53-related protein p73 has many functions similar to that of p53 including the ability to induce cell-cycle arrest and apoptosis. Both p53 and p73 function as transcription factors, and p73 activates expression of many genes that also are regulated by p53. Despite their similarities, it is evident that p53 and p73 are not interchangeable functionally, with p73 playing a role in normal growth and development that is not shared by p53. In this paper we describe the ability of p73β but not p53 to activate expression of the cyclin-dependent kinase inhibitor p57KIP and KvLQT1, two genes that are coregulated in an imprinted region of the genome. Our results suggest that p73 may regulate expression of genes through mechanisms that are not shared by p53, potentially explaining the different contributions of p53 and p73 to normal development.

Original languageEnglish
Pages (from-to)3529-3534
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume99
Issue number6
DOIs
Publication statusPublished - Mar 19 2002

ASJC Scopus subject areas

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