ArticleJournal of virology1994
Second-site long terminal repeat (LTR) revertants of replication-defective human immunodeficiency virus: effects of revertant TATA box motifs on virus infectivity, LTR-directed expression, in vitro RNA synthesis, and binding of basal transcription factors TFIID and TFIIA.
Article in Journal of virology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Early treatment regimens achieve sustained virologic remission in infant macaques infected with SIV at birth.Nature communications · 2022Article
- Regulation of Expression and Latency in BLV and HTLV.Viruses · 2020Review
- Effect of mimetic CDK9 inhibitors on HIV-1-activated transcription.Journal of molecular biology · 2013Article
- Use of ATP analogs to inhibit HIV-1 transcription.Virology · 2012Article
- CTGC motifs within the HIV core promoter specify Tat-responsive pre-initiation complexes.Retrovirology · 2012Article
- Inhibition of HIV Replication by Cyclic and Hairpin PNAs Targeting the HIV-1 TAR RNA Loop.Journal of nucleic acids · 2012Article
- Article
- Acetylated Tat regulates human immunodeficiency virus type 1 splicing through its interaction with the splicing regulator p32.Journal of virology · 2006Article
- Anti-HIV-1 activity of anti-TAR polyamide nucleic acid conjugated with various membrane transducing peptides.Nucleic acids research · 2005Article
- HIV-1 gene expression: lessons from provirus and non-integrated DNA.Retrovirology · 2004Review
- Promoter scanning for transcription inhibition with DNA-binding polyamides.Molecular and cellular biology · 2002Article
- Destabilization of tRNA3(Lys) from the primer-binding site of HIV-1 genome by anti-A loop polyamide nucleotide analog.Nucleic acids research · 2001Article
- HIV-1 tat induced apoptosis of T-cells is not mediated by TGF-beta.Medical oncology (Northwood, London, England) · 2000Article
- Cell cycle-regulated transcription by the human immunodeficiency virus type 1 Tat transactivator.Journal of virology · 2000Article
- Transcriptional up-regulation of the cyclin D2 gene and acquisition of new cyclin-dependent kinase partners in human T-cell leukemia virus type 1-infected cells.Journal of virology · 1999Article
- Interaction of human immunodeficiency virus type 1 Tat with a unique site of TFIID inhibits negative cofactor Dr1 and stabilizes the TFIID-TFIIA complex.Journal of virology · 1996Article
- Efficient transcription and replication of simian immunodeficiency virus in the absence of NF-kappaB and Sp1 binding elements.Journal of virology · 1996Article
- Sequential steps in Tat trans-activation of HIV-1 mediated through cellular DNA, RNA, and protein binding factors.Gene expression · 1996Article
- Human herpesvirus 6A ts suppresses both transformation by H-ras and transcription by the H-ras and human immunodeficiency virus type 1 promoters.Journal of virology · 1995Article
- Human immunodeficiency virus type 1 TAR element revertant viruses define RNA structures required for efficient viral gene expression and replication.Journal of virology · 1995Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Second-site revertants from replication-incompetent molecular clones of human immunodeficiency virus (HIV) contain base substitutions adjacent to the TATA motif. The altered TATA box motifs were analyzed for their effect(s) on virus infectivity, long terminal repeat (LTR)-directed expression in transient transfection assays, in vitro RNA synthesis, and assembly of the TFIID-TFIIA preinitiation complex. The revertant TATA boxes accelerated the kinetics of HIV replication when present in the context of an LTR containing a Sp1 mutation (deletion or site specific); no effect was observed on the infectivity of wild-type HIV. In chloramphenicol acetyltransferase assays and in vitro transcription systems, the altered TATA box motifs led to elevated basal levels of RNA synthesis from NF-kappa B- and Sp1-mutagenized and wild-type templates, respectively, but did not increase responsiveness to Tat transactivation. The revertant TATA boxes accelerated the binding of TFIID and TFIIA to the LTR and stabilized their association with the promoter. The revertants did not assemble a more-processive elongation complex. These results suggest that in the context of an impaired enhancer/promoter (viz., three mutated Sp1 elements), a series of HIV revertants emerge which contain LTR alterations that significantly augment basal RNA synthesis. The TATA motif revertants are capable of rescuing the enhancer/promoter defect and sustain virus infectivity.
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