HTLV-I tax induces cellular proteins that activate the kappa B element in the IL-2 receptor alpha gene

Science. 1988 Sep 23;241(4873):1652-5. doi: 10.1126/science.241.4873.1652.


Jurkat T cell lines constitutively expressing Tax, the 40-kilodalton transactivator protein of human T lymphotropic virus type I (HTLV-I), were used to investigate the mechanism by which this viral product deregulates the expression of the interleukin-2 receptor alpha gene (IL-2R alpha, Tac). Transfection of deleted forms of the IL-2R alpha promoter and in vitro DNA-binding studies revealed that a 12-base pair promoter segment, which has homology with the binding site for NF-kappa B, was required for Tax-induced activation of the IL-2R alpha promoter in vivo. An 18-base pair oligonucleotide containing this kappa B-like regulatory element proved sufficient to confer Tax inducibility upon a heterologous promoter. DNA affinity precipitation assays showed that Tax, like mitogenic stimuli, induced the expression of the 86-kilodalton cellular protein HIVEN86A, which specifically binds to the IL-2R alpha kappa B element in vitro. Furthermore, DNA/protein cross-linking studies revealed that several polypeptides interact with this sequence motif. Thus, the deregulation of IL-2R alpha gene expression encountered in HTLV-I leukemias appears to involve Tax activation of one or more cellular proteins that are normally induced by mitogens and that directly contribute to transcriptional activation of this receptor gene.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acetyltransferases / genetics
  • Cell Line
  • Chloramphenicol O-Acetyltransferase
  • DNA-Binding Proteins / biosynthesis*
  • DNA-Binding Proteins / physiology
  • Deltaretrovirus / genetics
  • Deltaretrovirus / physiology*
  • Gene Expression Regulation*
  • Nuclear Proteins / biosynthesis*
  • Nuclear Proteins / physiology
  • Plasmids
  • Promoter Regions, Genetic
  • Receptors, Antigen, T-Cell / genetics*
  • Receptors, Immunologic / genetics*
  • Receptors, Interleukin-2
  • Retroviridae Proteins / physiology*
  • Tetradecanoylphorbol Acetate / pharmacology
  • Trans-Activators
  • Transcription Factors / physiology*
  • Transfection
  • Viral Proteins / physiology*


  • DNA-Binding Proteins
  • Nuclear Proteins
  • Receptors, Antigen, T-Cell
  • Receptors, Immunologic
  • Receptors, Interleukin-2
  • Retroviridae Proteins
  • Trans-Activators
  • Transcription Factors
  • Viral Proteins
  • Acetyltransferases
  • Chloramphenicol O-Acetyltransferase
  • Tetradecanoylphorbol Acetate