Mechanisms of persistent NF-kappaB activation by HTLV-I tax

IUBMB Life. 2005 Feb;57(2):83-91. doi: 10.1080/15216540500078715.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Gene Expression Regulation, Neoplastic*
  • Gene Products, tax / metabolism*
  • Human T-lymphotropic virus 1 / metabolism*
  • Humans
  • Leukemia-Lymphoma, Adult T-Cell / metabolism*
  • Models, Biological*
  • NF-kappa B / metabolism*
  • Signal Transduction / physiology*


  • Gene Products, tax
  • NF-kappa B