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

Edward W. Harhaj, Nicole S. Harhaj

Research output: Contribution to journalReview articlepeer-review

38 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)83-91
Number of pages9
JournalIUBMB Life
Issue number2
StatePublished - Feb 2005
Externally publishedYes


  • Gene expression
  • Human T cell leukemia virus type I (HTLV-I)
  • NF-κB
  • NIK
  • Signal transduction
  • Tax
  • ikk
  • p100

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Genetics
  • Clinical Biochemistry
  • Cell Biology


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