ArticleProceedings of the National Academy of Sciences of the United States of America1999
Interactions between human cyclin T, Tat, and the transactivation response element (TAR) are disrupted by a cysteine to tyrosine substitution found in mouse cyclin T.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 120 citations in OpenAlex.
- Phosphorylation of CDK9 at Ser175 enhances HIV transcription and is a marker of activated P-TEFb in CD4(+) T lymphocytes.PLoS pathogens · 2013Trial
- HIV transgenic mouse monocytes display increasedJournal of virology · 2026Article
- Drug design for cyclin-dependent kinase 9 (CDK9) inhibitorsBiochemistry and biophysics reports · 2025Article
- The HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- A Truncated Isoform of Cyclin T1 Could Contribute to the Non-Permissive HIV-1 Phenotype of U937 Promonocytic Cells.Viruses · 2024Article
- P-TEFb: The master regulator of transcription elongation.Molecular cell · 2023Review
- Identification of Novel Nucleocapsid Chimeric Proteins Inhibiting HIV-1 Replication.International journal of molecular sciences · 2022Article
- Identification of a novel CDK9 inhibitor targeting the intramolecular hidden cavity of CDK9 induced by Tat binding.PloS one · 2022Article
- Biogenesis of P-TEFb in CD4+ T cells to reverse HIV latency is mediated by protein kinase C (PKC)-independent signaling pathways.PLoS pathogens · 2021Article
- P-TEFb as A Promising Therapeutic Target.Molecules (Basel, Switzerland) · 2020Review
- Fused in sarcoma silences HIV gene transcription and maintains viral latency through suppressing AFF4 gene activation.Retrovirology · 2019Article
- HEXIM1-Tat chimera inhibits HIV-1 replication.PLoS pathogens · 2018Article
- Cyclophilin A enables specific HIV-1 Tat palmitoylation and accumulation in uninfected cells.Nature communications · 2018Article
- HIV Tat/P-TEFb Interaction: A Potential Target for Novel Anti-HIV Therapies.Molecules (Basel, Switzerland) · 2018Review
- MD simulation of the Tat/Cyclin T1/CDK9 complex revealing the hidden catalytic cavity within the CDK9 molecule upon Tat binding.PloS one · 2017Article
- HIV-tat alters Connexin43 expression and trafficking in human astrocytes: role in NeuroAIDS.Journal of neuroinflammation · 2016Article
- Postentry restriction of Mason-Pfizer monkey virus in mouse cells.Journal of virology · 2015Article
- Molecular dynamics simulation and experimental verification of the interaction between cyclin T1 and HIV-1 Tat proteins.PloS one · 2015Article
- Short chain fatty acids potently induce latent HIV-1 in T-cells by activating P-TEFb and multiple histone modifications.Virology · 2015Article
- Genetic analysis of the structure and function of 7SK small nuclear ribonucleoprotein (snRNP) in cells.The Journal of biological chemistry · 2014Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional transactivator Tat from HIV binds to the transactivation response element (TAR) RNA to increase rates of elongation of viral transcription. Human cyclin T supports these interactions between Tat and TAR. In this study, we report the sequence of mouse cyclin T and identify the residues from positions 1 to 281 in human cyclin T that bind to Tat and TAR. Mouse cyclin T binds to Tat weakly and is unable to facilitate interactions between Tat and TAR. Reciprocal exchanges of the cysteine and tyrosine at position 261 in human and mouse cyclin T proteins also render human cyclin T inactive and mouse cyclin T active. These findings reveal the molecular basis for the restriction of Tat transactivation in rodent cells.
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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.