These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: 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.
    Author: Suzuki T, Hirai H, Yoshida M.
    Journal: Oncogene; 1994 Nov; 9(11):3099-105. PubMed ID: 7936632.
    Abstract:
    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.
    [Abstract] [Full Text] [Related] [New Search]