Tax induces nuclear translocation of NF-kappa B through dissociation of cytoplasmic complexes containing p105 or p100 but does not induce degradation of I kappa B alpha/MAD3.

摘要: The activity of the NF-kappa B transcription factor is controlled through cytoplasmic retention by either two types molecules: inhibitor I kappa alpha/MAD3 or p105 and p100 precursors p50 p52 DNA-binding subunits. Treatment cells with classical inducers such as tumor necrosis factor, interleukin-1, phorbol myristate acetate, lipopolysaccharide results in MAD3 degradation followed nuclear translocation B. On other hand, mechanisms involved dissociation p105/p100-containing complexes are largely unknown. Tax protein encoded human T-cell leukemia virus type 1 a potent activator viral cellular gene transcription. It does not bind DNA directly but seems to activate indirectly enhancing activities factors that recognize responsive elements located promoters Tax-responsive genes forming ternary these DNA. has been previously shown able induce We demonstrate here can members family retained cytoplasm their interaction p100. induces no apparent MAD3, although experiments using cycloheximide indicate it decreases half-life MAD3. However, this shared mutant which unable These suggest activates essentially p105/p100 pathway.