Tax protein of HTLV-1 interacts with the Rel homology domain of NF-kappa B p65 and c-Rel proteins bound to the NF-kappa B binding site and activates transcription.

Tax protein of human T cell leukemia virus type 1 (HTLV-1) enhances transcription of several cellular genes through activation of a specific enhancer, the NF-kappa B binding site. We found previously that Tax binds to NF-kappa B p50, which is a member of the Rel/NF-kappa B family proteins, and associates with the DNA sequence of the NF-kappa B binding site. In the present study, we tested other NF-kappa B family proteins and found that NF-kappa B p65 and c-Rel proteins also bind to Tax and that their complexes with Tax bind to the DNA sequence of the NF-kappa B binding site. The Tax binding site on NF-kappa B p50 is the Rel homology domain, which is conserved in the Rel/NF-kappa B family proteins. The formations of these complexes by Tax mutants were well correlated with their transactivating capacities. In F9 embryonic carcinoma cells, Tax enhanced transcription synergistically with NF-kappa B p65 or c-Rel. Thus Tax interacts with the Rel homology domain of Rel/NF-kappa B family proteins which bind to the NF-kappa B binding site and activates transcription.