ArticleNucleic acids research1996
Activation domains of transcription factors mediate replication dependent transcription from a minimal HIV-1 promoter.
Article in Nucleic acids research, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- The HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- Involvement of Human Cellular Proteins and Structures in Realization of the HIV Life Cycle: A Comprehensive Review, 2024.Viruses · 2024Review
- The sly-miR166-SlyHB module acts as a susceptibility factor during ToLCNDV infection.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2022Article
- Cell-cycle dependence of transcription dominates noise in gene expression.PLoS computational biology · 2013Article
- Expression of human endogenous retrovirus type K (HML-2) is activated by the Tat protein of HIV-1.Journal of virology · 2012Article
- Antagonistic effects of T-Ag and VP16 reveal a role for RNA pol II elongation on alternative splicing.The EMBO journal · 2001Article
- Interference of the simian virus 40 origin of replication by the cytomegalovirus immediate early gene enhancer: evidence for competition of active regulatory chromatin conformation in a single domain.Molecular and cellular biology · 2000Article
- Regulation of HIV-1 transcription.Gene expression · 1999Review
- Poly(A)-driven and poly(A)-assisted termination: two different modes of poly(A)-dependent transcription termination.Molecular and cellular biology · 1998Article
- Transcription and polyadenylation in a short human intergenic region.Nucleic acids research · 1997Article
- Differential in vivo activation of the class II and class III snRNA genes by the POU-specific domain of Oct-1.Nucleic acids research · 1997Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Transcription from a minimal HIV-1 promoter containing the three Sp1 binding sites and TATA box can be activated without Tat by template DNA replication. Here we show that this activation can also be mediated by recombinant GAL4 fusion proteins containing the activation domains of Sp1, VP16 or CTF (or by full-length GAL4) targeted to the HIV-1 promoter by replacing the Sp1 sites with five GAL4 binding sites. Thus Sp1 is not unique in its ability to mediate replication activated transcription, although the degree of processivity elicited by the different activators varied significantly from strongly processive (GAL4-VP16) to relatively non-processive (GAL4-Sp1 or -CTF). Processive GAL4-VP16-activated transcription, but not efficient initiation, required multiple GAL4 binding sites. In the presence of Tat, transcription with GAL4-SP1 and GAL4-CTF was further activated (principally at the level of processivity) but GAL4-VP16-potentiated transcription was only slightly stimulated. The Tat-dependent switch from non-processive to fully processive transcription was particularly marked for GAL4-Sp1, an effect which may be relevant to the selection of Sp1 binding sites by the HIV-1 promoter.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.