AJTR Copyright © 2009-All rights reserved. Published by e-Century Publishing Corporation, Madison, WI 53711
Am J Translational Res 2010;2(1):56-64

Review Article
Arrest-defective-1 protein (ARD1): tumor suppressor or oncoprotein?

Yong Liao, Mien-Chie Hung

Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Houston,
TX 77030, USA; Graduate School of Biomedical Sciences, The University of Texas Health Science Center,
Houston, TX 77030, USA; Center for Molecular Medicine and Graduate Institute of Cancer Biology, China Medical
University and Hospital, Taichung 404, Taiwan; Asia University, Taichung 413, Taiwan.

Received December 10, 2009; accepted December 18, 2009; available online January 1, 2009

Abstract: Arrest-defect-1 protein (ARD1), an acetyltransferase, catalyzes N-alpha-acetylation in yeast. In
mammalian cells, both N-alpha-acetylation and -acetylation induced by ARD1 have been reported. Emerging
evidence has revealed that ARD1 is involved in a variety of cellular functions, including proliferation, apoptosis,
autophagy, and differentiation and that dysregulation of ARD1 is associated with tumorigenesis and
neurodegenerative disorder. This review will discuss recent discoveries regarding variations among the different
ARD1 isoforms, the associated biological functions of ARD1, and ARD1 localization in different cells. We will also
discuss the potential upstream regulators and downstream targets of ARD1 to provide new avenues for resolving
its controversial roles in cancer development. (AJTR912003).

Key words: ARD1, acetyltransferase, acetylation, tumorigenesis

Full Text  PDF

Address all correspondence to:
Mien-Chie Hung, PhD,
Department of Molecular & Cellular Oncology
The University of Texas M.D. Anderson Cancer Center
1515 Holcombe Blvd.
TX 77030, USA;
Tel: 713-792-3668
E-mail:
mhung@mdanderson.org.