ArticleJournal of virology2002
Optimized chimeras between kinase-inactive mutant Cdk9 and truncated cyclin T1 proteins efficiently inhibit Tat transactivation and human immunodeficiency virus gene expression.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV Therapies.Molecules (Basel, Switzerland) · 2018Review
- P-TEFb goes viral.Inside the cell · 2016Review
- Visualization of positive transcription elongation factor b (P-TEFb) activation in living cells.The Journal of biological chemistry · 2015Article
- Molecular dynamics simulation and experimental verification of the interaction between cyclin T1 and HIV-1 Tat proteins.PloS one · 2015Article
- Genetic analysis of the structure and function of 7SK small nuclear ribonucleoprotein (snRNP) in cells.The Journal of biological chemistry · 2014Article
- Impact of Tat Genetic Variation on HIV-1 Disease.Advances in virology · 2012Article
- Ser-634 and Ser-636 of Kaposi's Sarcoma-Associated Herpesvirus RTA are Involved in Transactivation and are Potential Cdk9 Phosphorylation Sites.Frontiers in microbiology · 2012Article
- Patient mutation in AIRE disrupts P-TEFb binding and target gene transcription.Nucleic acids research · 2011Article
- The positive transcription elongation factor b is an essential cofactor for the activation of transcription by myocyte enhancer factor 2.Journal of molecular biology · 2008Article
- Dominant negative mutant cyclin T1 proteins inhibit HIV transcription by specifically degrading Tat.Retrovirology · 2008Article
- Regulation of HIV-1 latency by T-cell activation.Cytokine · 2007Review
- Transcriptional profiles of latent human immunodeficiency virus in infected individuals: effects of Tat on the host and reservoir.Journal of virology · 2003Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The human cyclin T1 (hCycT1) protein from the positive transcription elongation factor b (P-TEFb) binds the transactivator Tat and the transactivation response (TAR) RNA stem loop from human immunodeficiency virus type 1 (HIV). This complex activates the elongation of viral transcription. To create effective inhibitors of Tat and thus HIV replication, we constructed mutant hCycT1 proteins that are defective in binding its kinase partner, Cdk9, or TAR. Although these mutant hCycT1 proteins did not increase Tat transactivation in murine cells, their dominant-negative effects were small in human cells. Higher inhibitory effects were obtained when hCycT1 was fused with the mutant Cdk9 protein. Since the autophosphorylation of the C terminus of Cdk9 is required for the formation of the stable complex between P-TEFb, Tat, and TAR, these serines and threonines were changed to glutamate in a kinase-inactive Cdk9 protein. This chimera inhibited Tat transactivation and HIV gene expression in human cells. Therefore, this dominant-negative kinase-inactive mutant Cdk9.hCycT1 chimera could be used for antiviral gene therapy.
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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.