Document 0494 DOCN M9550494 TI Functional similarities between HIV-1 Tat and DNA sequence-specific transcriptional activators. DT 9505 AU Madore SJ; Cullen BR; Howard Hughes Medical Institute, Duke University Medical Center,; Durham, North Carolina 27710. SO Virology. 1995 Feb 1;206(2):1150-4. Unique Identifier : AIDSLINE MED/95159430 AB 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. DE Animal Binding Sites Cell Line Cercopithecus aethiops Comparative Study Cytomegalovirus/GENETICS/METABOLISM DNA, Viral/*METABOLISM Gene Products, tat/*METABOLISM Human *HIV Long Terminal Repeat HIV-1/GENETICS/*METABOLISM Kidney NF-kappa B/METABOLISM Plasmids Promoter Regions (Genetics) Recombinant Fusion Proteins/METABOLISM Trans-Activation (Genetics) Trans-Activators/*METABOLISM Transcription Factor, Sp1/METABOLISM Transcription, Genetic Transfection JOURNAL ARTICLE SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).