Abstract:
:The Tat regulatory protein encoded by human immunodeficiency virus type 1 (HIV-1) induces high levels of transcription from the viral long terminal repeat (LTR) promoter element after interacting with a promoter proximal RNA target sequence. In the wild-type HIV-1 LTR, this activation is facilitated by the synergistic interaction of Tat with the NF-kappa B and, particularly, SP1 regulatory proteins that bind to DNA sequences within the LTR promoter element. Using a synthetic Tat responsive indicator construct, we here demonstrate that NF-kappa B and SP1 are not uniquely or even unusually competent to synergize with HIV-1 Tat. Instead, these proteins can be functionally replaced by several, but not all, of the heterologous cellular and viral transcriptional activators tested. Tat therefore shares the ability to functionally synergize with a range of transcriptional activators, which is characteristic of DNA-sequence-specific regulatory proteins.
journal_name
Virologyjournal_title
Virologyauthors
Madore SJ,Cullen BRdoi
10.1006/viro.1995.1041subject
Has Abstractpub_date
1995-02-01 00:00:00pages
1150-4issue
2eissn
0042-6822issn
1096-0341pii
S0042-6822(85)71041-0journal_volume
206pub_type
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