¹Institute for Cancer Genetics, Department of Pathology, College of Physicians & Surgeons, Columbia University, 1150 St Nicholas Ave, New York, NY 10032, USA

Correspondence: Dr W Gu, E-mail: wg8@columbia.edu

Received 21 November 2005; Revised 21 March 2006; Accepted 29 March 2006; Published online 25 April 2006.

Abstract

In this review, we discuss the recent identification of ARF-BP1 (also known as Mule, UREB1, E3^histone, LASU1, and HectH9). ARF-BP1, a HECT domain-containing E3 ubiquitin ligase, interacts with ARF and p53. Its ubiquitin ligase activity is inhibited by ARF. Inactivation of ARF-BP1 stabilised p53 and induced apoptosis. Notably, inactivation of ARF-BP1 also caused cell growth repression in p53-null cells and breast cancer cells with mutant p53. Thus, ARF-BP1 emerges as a novel therapeutic target against cancer regardless of p53 status.