ReviewRetrovirology2005
Tat gets the "green" light on transcription initiation.
Review in Retrovirology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
84 citing papers in PubMed, 149 citations in OpenAlex.
- Versatile HIV Rev-dependent reporter cell system for stringent and sensitive quantification of viral reservoirs, neutralizing antibodies, and restriction factors.Retrovirology · 2026Article
- Versatile HIV Rev-dependent reporter cell system for stringent and sensitive quantification of viral reservoirs, neutralizing antibodies, and restriction factors.bioRxiv : the preprint server for biology · 2025Article
- FUBP3 enhances HIV-1 transcriptional activity and regulates immune response pathways in T cells.Molecular therapy. Nucleic acids · 2025Article
- The snakehead retrovirus promoter functions independently of the 3'ORF protein and its products are maternally inherited in transgenic zebrafish.PLoS pathogens · 2025Article
- Human chromatin remodelers regulating HIV-1 transcription: a target for small molecule inhibitors.Epigenetics & chromatin · 2025Review
- Nanoparticle delivery of Tat synergizes with classical latency reversal agents to express HIV antigen targets.Antimicrobial agents and chemotherapy · 2024Article
- The chaperone protein p32 stabilizes HIV-1 Tat and strengthens the p-TEFb/RNAPII/TAR complex promoting HIV transcription elongation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Cure and Long-Term Remission Strategies.Methods in molecular biology (Clifton, N.J.) · 2022Review
- Block-And-Lock: New Horizons for a Cure for HIV-1.Viruses · 2020Review
- Mutations altering acetylated residues in the CTD of HIV-1 integrase cause defects in proviral transcription at early times after integration of viral DNA.PLoS pathogens · 2020Article
- NMR Studies of Retroviral Genome Packaging.Viruses · 2020Review
- Review
- Genetic variation and function of the HIV-1 Tat protein.Medical microbiology and immunology · 2019Review
- A cis-Acting Element Downstream of the Mouse Mammary Tumor Virus Major Splice Donor Critical for RNA Elongation and Stability.Journal of molecular biology · 2018Article
- Cellular RelB interacts with the transactivator Tat and enhance HIV-1 expression.Retrovirology · 2018Article
- Modeling the Function of TATA Box Binding Protein in Transcriptional Changes Induced by HIV-1 Tat in Innate Immune Cells and the Effect of Methamphetamine Exposure.Frontiers in immunology · 2018Article
- The Use of Tricyclo-DNA Oligomers for the Treatment of Genetic Disorders.Biomedicines · 2017Review
- Tat is a multifunctional viral protein that modulates cellular gene expression and functions.Oncotarget · 2017Review
- Identification of HIV-1 Tat-Associated Proteins Contributing to HIV-1 Transcription and Latency.Viruses · 2017Article
- Functional Studies of CCAAT/Enhancer Binding Protein Site Located Downstream of the Transcriptional Start Site.Clinical medicine insights. Pathology · 2017Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Human immunodeficiency virus type 1 (HIV-1) Tat transactivation is an essential step in the viral life cycle. Over the past several years, it has become widely accepted that Tat exerts its transcriptional effect by binding the transactivation-responsive region (TAR) and enhancing transcriptional elongation. Consistent with this hypothesis, it has been shown that Tat promotes the binding of P-TEFb, a transcription elongation factor composed of cyclin T1 and cdk9, and the interaction of Tat with P-TEFb and TAR leads to hyperphosphorylation of the C-terminal domain (CTD) of RNA Pol II and increased processivity of RNA Pol II. A recent report, however, has generated renewed interest that Tat may also play a critical role in transcription complex (TC) assembly at the preinitiation step. Using in vivo chromatin immunoprecipitation assays, the authors reported that the HIV TC contains TBP but not TBP-associated factors. The stimulatory effect involved the direct interaction of Tat and P-TEFb and was evident at the earliest step of TC assembly, the TBP-TATA box interaction. In this article, we will review this data in context of earlier data which also support Tat's involvement in transcriptional complex assembly. Specifically, we will discuss experiments which demonstrated that Tat interacted with TBP and increased transcription initiation complex stability in cell free assays. We will also discuss studies which demonstrated that over expression of TBP alone was sufficient to obtain Tat activated transcription in vitro and in vivo. Finally, studies using self-cleaving ribozymes which suggested that Tat transactivation was not compatible with pausing of the RNA Pol II at the TAR site will be discussed.
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What OpenQuestion holds
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.