Tax Protein of Human T-cell Leukemia Virus Type I Binds to the Ankyrin Motifs of Inhibitory Factor Kappa B and Induces Nuclear Translocation of Transcription Factor NF-kappa B Proteins for Transcriptional Activation

Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3584-8. doi: 10.1073/pnas.91.9.3584.


Human T-cell leukemia virus type I causes adult T-cell leukemia and tropical spastic paraparesis, and its regulator protein Tax has been implicated in the pathogenic activity of human T-cell leukemia virus type I. Tax activates transcription of viral and cellular genes through specific enhancers: the 21-bp enhancer of human T-cell leukemia virus type I, the nuclear factor kappa B (NF-kappa B)-binding site of the interleukin 2 receptor alpha gene, and the serum-responsive element of c-fos. Tax binds to enhancer-binding proteins including cAMP-responsive element-binding protein, cAMP-responsive element modulator, transcription factor NF-kappa B p50 and p67SRF, and associates with each enhancer DNA indirectly. In addition to this mechanism, we report here that Tax binds to inhibitory factor kappa B gamma (I-kappa B) gamma, which forms a complex with NF-kappa B protein heterodimer p50-p65 or homodimer p50-p50 and retains them in the cytoplasm. Tax binding to I-kappa B gamma induces nuclear translocation of NF-kappa B p65. In association with this nuclear translocation of p65, transcription directed by the kappa B enhancer is strongly activated. Tax binds to the ankyrin motifs of I-kappa B gamma, suggesting its possible interaction with many other proteins carrying ankyrin motifs contributing to various regulatory processes. This is a different mechanism of transcriptional activation by the oncoprotein Tax and seems to be independent from the trans-activation through indirect binding to enhancer DNAs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Binding Sites
  • Cell Nucleus / metabolism
  • Gene Expression Regulation, Viral*
  • Gene Products, tax / metabolism*
  • Human T-lymphotropic virus 1 / genetics*
  • Mice
  • NF-kappa B / metabolism*
  • Protein Binding
  • Proto-Oncogene Proteins / metabolism*
  • Transcription Factor RelB
  • Transcription Factors*
  • Transcription, Genetic


  • Gene Products, tax
  • NF-kappa B
  • Proto-Oncogene Proteins
  • Relb protein, mouse
  • Transcription Factors
  • Transcription Factor RelB