Review
Copyright ©2010 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Biol Chem. Jan 26, 2010; 1(1): 13-20
Published online Jan 26, 2010. doi: 10.4331/wjbc.v1.i1.13
Role of post-translational modifications of HTLV-1 Tax in NF-κB activation
Noula Shembade, Edward W Harhaj
Noula Shembade, Edward W Harhaj, Department of Microbiology and Immunology, Sylvester Comprehensive Cancer Center, University of Miami, Miller School of Medicine, Miami, FL 33136, United States
Author contributions: Shembade N and Harhaj EW wrote and revised the manuscript.
Supported by Grants from the United States Public Health Service/National Institutes of Health, No. RO1CA135362, RO1GM083143 and PO1CA128115
Correspondence to: Noula Shembade, PhD, Assistant Professor, Department of Microbiology and Immunology, Sylvester Comprehensive Cancer Center, University of Miami School of Medicine, Room 519, Papanicolaou Building, 1550 NW 10th Ave, Miami, FL 33136, United States. nshembade@med.miami.edu
Telephone: +1-305-2437894 Fax: +1-305-2436410
Received: November 6, 2009
Revised: December 17, 2009
Accepted: December 24, 2009
Published online: January 26, 2010
Abstract

Human T-cell leukemia virus type 1 (HTLV-1), the first human retrovirus discovered, is the etiological agent of adult-T-cell leukemia/lymphoma. The HTLV-1 encoded Tax protein is a potent oncoprotein that deregulates gene expression by constitutively activating nuclear factor-κB (NF-κB). Tax activation of NF-κB is critical for the immortalization and survival of HTLV-1-infected T cells. In this review, we summarize the present knowledge on mechanisms underlying Tax-mediated NF-κB activation, with an emphasis on post-translational modifications of Tax.

Keywords: Adult-T-cell leukemia/lymphoma; Human T-cell leukemia virus type 1; Nuclear factor-κB; Human T-cell leukemia virus type 1-associated myelopathy/tropical spastic paraparesis; IKK