Regulation of gene expression by HTLV-I Tax protein

Methods. 1998 Sep;16(1):83-94. doi: 10.1006/meth.1998.0646.


The human T-cell leukemia virus type I or HTLV-I is the causative agent of adult T-cell leukemia. A protein encoded by HTLV-I, Tax, activates viral gene expression and is essential for transforming T-lymphocytes. Tax activates HTLV-I gene expression via interactions with the ATF/CREB proteins and the coactivators CBP/p300 which assemble as a multiprotein complex on regulatory elements known as 21-bp repeats in the HTLV-I LTR. Tax can also activate expression from cellular genes including the interleukin-2 (IL-2) and the IL-2 receptor genes via increases in nuclear levels of NF-kappaB. Tax modulation of gene expression via the ATF/CREB and NF-kappaB pathways is linked to its transforming properties. This review discusses the mechanisms by which Tax regulates viral and cellular gene expression.

Publication types

  • Review

MeSH terms

  • Cyclic AMP Response Element-Binding Protein / metabolism
  • Enhancer Elements, Genetic / genetics
  • Gene Expression Regulation, Viral / genetics*
  • Gene Products, tax / physiology*
  • HIV-1 / genetics*
  • Histone Acetyltransferases
  • Humans
  • NF-kappa B / physiology
  • Nuclear Receptor Coactivator 3
  • Promoter Regions, Genetic / genetics
  • Trans-Activators / metabolism
  • Transcriptional Activation / genetics
  • Viral Proteins / genetics*


  • Cyclic AMP Response Element-Binding Protein
  • Gene Products, tax
  • NF-kappa B
  • Trans-Activators
  • Viral Proteins
  • Histone Acetyltransferases
  • NCOA3 protein, human
  • Nuclear Receptor Coactivator 3