       Document 0417
 DOCN  M9640417
 TI    Activation of NF-kappa B by the Tax protein of HTLV-1.
 DT    9604
 AU    Munoz E; Israel A; Unite de Biologie Moleculaire de l'Expression
       Genique,; Institut Pasteur, Paris, France.
 SO    Immunobiology. 1995 Jul;193(2-4):128-36. Unique Identifier : AIDSLINE
       MED/96030032
 AB    The Tax protein, encoded by the human T cell leukemia virus HTLV-1, is
       responsible for transcriptional activation of the viral genome through
       conserved 21bp repeats located in its promoter. Tax also activates the
       transcription of cellular genes such as interleukin 2, interleukin 2
       receptor (IL2R), GM-CSF, vimentin, c-fos, c-jun as well as the major
       histocompatibility complex class I genes. Tax does not bind DNA
       directly, but seems to activate transcription indirectly by enhancing
       the activity of the transcription factors that recognize responsive
       elements located in the promoters of the Tax-responsive genes, or by
       forming ternary complexes with these factors and DNA. One class of
       target sites for Tax are the kappa B sequences which are bound by
       members of the rel/NF-kappa B family. It has been previously shown that
       Tax is able to induce nuclear translocation of NF-kappa B. The activity
       of the NF-kappa B transcription factor is normally controlled through
       cytoplasmic retention by either of two types of molecules: the inhibitor
       I kappa B alpha/MAD3 or the p105 and p100 precursors of the p50 and p52
       DNA-binding subunits. Treatment of cells with classical NF-kappa B
       inducers like TNF, IL-1, PMA or LPS results in MAD-3 degradation
       followed by nuclear translocation of NF-kappa B. On the other hand, the
       mechanisms involved in the dissociation of the cytoplasmic
       p105/p100-containing complexes are largely unknown. We demonstrate here
       that Tax can induce translocation of members of the NF-kappa B family
       retained in the cytoplasm through interaction with either p105 or p100.
       On the other hand Tax induces no apparent degradation of MAD-3. These
       results suggest that Tax activates NF-kappa B essentially through the
       p105/p100-retention pathway.
 DE    Animal  Gene Products, tax/*PHYSIOLOGY  Human
       HTLV-I/CHEMISTRY/*GENETICS  NF-kappa B/*GENETICS  Support, Non-U.S.
       Gov't  Trans-Activation (Genetics)/*IMMUNOLOGY  JOURNAL ARTICLE  REVIEW
       REVIEW, TUTORIAL

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

