Document 0040
 DOCN  M9460040
 TI    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.
 DT    9408
 AU    Hirai H; Suzuki T; Fujisawa J; Inoue J; Yoshida M; Department of
       Cellular and Molecular Biology, University of; Tokyo, Japan.
 SO    Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3584-8. Unique Identifier :
       AIDSLINE MED/94224784
 AB    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.
 DE    Animal  Binding Sites  Cell Nucleus/METABOLISM  *Gene Expression
       Regulation, Viral  Gene Products, tax/*METABOLISM  HTLV-I/*GENETICS
       Mice  NF-kappa B/*METABOLISM  Protein Binding  Proto-Oncogene
       Proteins/*METABOLISM  Support, Non-U.S. Gov't  Transcription, Genetic
       JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
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