ArticleGenes & development1998
The interaction between HIV-1 Tat and human cyclin T1 requires zinc and a critical cysteine residue that is not conserved in the murine CycT1 protein.
Article in Genes & development, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 220 papers.
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Who cites it
220 citing papers in PubMed, 428 citations in OpenAlex.
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- 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
- Monocyte to macrophage differentiation and changes in cellular redox homeostasis promote cell type-specific HIV latency reactivation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The cell biology of HIV-1 latency and rebound.Retrovirology · 2024Review
- Enhanced NF-κB activation via HIV-1 Tat-TRAF6 cross-talk.Science advances · 2024Article
- HIV-2 inhibits HIV-1 gene expression via two independent mechanisms during cellular co-infection.Journal of virology · 2023Article
- A CRISPR Screen of HIV Dependency Factors Reveals ThatViruses · 2023Article
- Identification of Novel Nucleocapsid Chimeric Proteins Inhibiting HIV-1 Replication.International journal of molecular sciences · 2022Article
- Productive Replication of HIV-1 but Not SIVmac in Small Ruminant Cells.Pathogens (Basel, Switzerland) · 2022Article
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- 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
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- Childhood HIV-associated nephropathy: 36 years later.Pediatric nephrology (Berlin, Germany) · 2021Review
- CDK9: A Comprehensive Review of Its Biology, and Its Role as a Potential Target for Anti-Cancer Agents.Frontiers in oncology · 2021Review
- An HIV-Tat inducible mouse model system of childhood HIV-associated nephropathy.Disease models & mechanisms · 2020Article
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- Review
160 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
HIV-1 Tat activates transcription through binding to human cyclin T1, a regulatory subunit of the TAK/P-TEFb CTD kinase complex. Here we show that the cyclin domain of hCycT1 is necessary and sufficient to interact with Tat and promote cooperative binding to TAR RNA in vitro, as well as mediate Tat transactivation in vivo. A Tat:TAR recognition motif (TRM) was identified at the carboxy-terminal edge of the cyclin domain, and we show that hCycT1 can interact simultaneously with Tat and CDK9 on TAR RNA in vitro. Alanine-scanning mutagenesis of the hCycT1 TRM identified residues that are critical for the interaction with Tat and others that are required specifically for binding of the complex to TAR RNA. Interestingly, we find that the interaction between Tat and hCycT1 requires zinc as well as essential cysteine residues in both proteins. Cloning and characterization of the murine CycT1 protein revealed that it lacks a critical cysteine residue (C261) and forms a weak, zinc-independent complex with HIV-1 Tat that greatly reduces binding to TAR RNA. A point mutation in mCycT1 (Y261C) restores high-affinity, zinc-dependent binding to Tat and TAR in vitro, and rescues Tat transactivation in vivo. Although overexpression of hCycT1 in NIH3T3 cells strongly enhances transcription from an integrated proviral promoter, we find that this fails to overcome all blocks to productive HIV-1 infection in murine 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.