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Mechanisms of Persistent NF‐κB Activation by HTLV‐I Tax
Author(s) -
Harhaj Edward W.,
Harhaj Nicole S.
Publication year - 2005
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216540500078715
Subject(s) - nf κb , signal transduction , mechanism (biology) , cancer research , pathogenesis , biology , leukemia , human t lymphotropic virus 1 , signal transducing adaptor protein , t cell leukemia , microbiology and biotechnology , immunology , philosophy , epistemology
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‐κB. Tax activation of NF‐κB 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‐κB signaling pathways. The adaptor function of Tax appears to be a common and important mechanism for the pathological activation of both NF‐κB pathways.IUBMB Life, 57: 83‐91, 2005