Mechanisms of persistent NF-kappaB activation by HTLV-I tax.
Human T cell leukemia virus type I (HTLV-I) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL). The HTLV-I Tax protein is thought to play a significant role in the initiation and pathogenesis of HTLV-I-mediated disease. Tax is a potent oncogene that deregulates cellular gene expression by persistently activating signaling pathways such as NF-kappaB. Tax activation of NF-kappaB is critical for the immortalization and survival of HTLV-I-infected T cells. In this review, we describe recent insights into the mechanisms employed by Tax to activate the canonical and noncanonical NF-kappaB signaling pathways. The adaptor function of Tax appears to be a common and important mechanism for the pathological activation of both NF-kappaB pathways.
Harhaj
Edward W
EW
Department of Microbiology and Immunology, Sylvester Comprehensive Cancer Center, The University of Miami School of Medicine, Miami, FL 33136, USA. eharhaj@med.miami.edu
Harhaj
Nicole S
NS
D015972:Gene Expression Regulation, Neoplastic; D016356:Gene Products, tax / Q000378:metabolism*; D015368:Human T-lymphotropic virus 1 / Q000378:metabolism*; D006801:Humans; D015459:Leukemia-Lymphoma, Adult T-Cell / Q000378:metabolism*; D008954:Models, Biological; D016328:NF-kappa B / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*
D016356:Gene Products, tax; D016328:NF-kappa B