Inhibition of tax-mediated increase in DNA binding

摘要

The Tax protein of Human T Cell Leukemia Virus Type 1 (HTLV-I) transcriptionally activated the HTLV-I promoter through binding sites for ATF, a family of cellular bZIP transcription factors. In this disclosure, it is reported that Tax dramatically increases the in vitro DNA binding activity of multiple ATF proteins. Tax also stimulates DNA binding of related bZIP proteins but does not affect the activity of proteins lacking a bZIP domain. The increased DNA binding activity occurs by a novel mechanism in which Tax promotes homodimerization in the absence of DNA. The elevated concentration of the bZIP homodimer results in increased DNA binding.