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).
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: firstname.lastname@example.org.