ArticleMolecular and cellular biology2000
Relief of two built-In autoinhibitory mechanisms in P-TEFb is required for assembly of a multicomponent transcription elongation complex at the human immunodeficiency virus type 1 promoter.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 86 citations in OpenAlex.
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- The HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- CDK9: A Comprehensive Review of Its Biology, and Its Role as a Potential Target for Anti-Cancer Agents.Frontiers in oncology · 2021Review
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- Human Tat-specific factor 1 binds the HIV-1 genome and selectively transports HIV-1 RNAs.Molecular biology reports · 2020Article
- The pre-mRNA splicing and transcription factor Tat-SF1 is a functional partner of the spliceosome SF3b1 subunit via a U2AF homology motif interface.The Journal of biological chemistry · 2019Article
- The HIV-1 Tat Protein Enhances Splicing at the Major Splice Donor Site.Journal of virology · 2018Article
- The BET inhibitor OTX015 reactivates latent HIV-1 through P-TEFb.Scientific reports · 2016Article
- Hsp90 in Cancer: Transcriptional Roles in the Nucleus.Advances in cancer research · 2016Review
- HIV-1 Tat second exon limits the extent of Tat-mediated modulation of interferon-stimulated genes in antigen presenting cells.Retrovirology · 2014Article
- Tip110 protein binds to unphosphorylated RNA polymerase II and promotes its phosphorylation and HIV-1 long terminal repeat transcription.The Journal of biological chemistry · 2014Article
- Enforcing the pause: transcription factor Sp3 limits productive elongation by RNA polymerase II.Cell cycle (Georgetown, Tex.) · 2013Article
- Review
- The BET bromodomain inhibitor JQ1 activates HIV latency through antagonizing Brd4 inhibition of Tat-transactivation.Nucleic acids research · 2013Article
- Transition step during assembly of HIV Tat:P-TEFb transcription complexes and transfer to TAR RNA.Molecular and cellular biology · 2012Article
- RNA polymerase II elongation control.Annual review of biochemistry · 2012Review
- The CDK9/cyclin T1 subunits of P-TEFb in mouse oocytes and preimplantation embryos: a possible role in embryonic genome activation.BMC developmental biology · 2011Article
- G-actin participates in RNA polymerase II-dependent transcription elongation by recruiting positive transcription elongation factor b (P-TEFb).The Journal of biological chemistry · 2011Article
- Identification of Tat-SF1 cellular targets by exon array analysis reveals dual roles in transcription and splicing.RNA (New York, N.Y.) · 2011Article
- CYCLINg through transcription: posttranslational modifications of P-TEFb regulate transcription elongation.Cell cycle (Georgetown, Tex.) · 2010Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
Tat stimulation of human immunodeficiency virus type 1 (HIV-1) transcription requires Tat-dependent recruitment of human positive transcription elongation factor b (P-TEFb) to the HIV-1 promoter and the formation on the trans-acting response element (TAR) RNA of a P-TEFb-Tat-TAR ternary complex. We show here that the P-TEFb heterodimer of Cdk9-cyclin T1 is intrinsically incapable of forming a stable complex with Tat and TAR due to two built-in autoinhibitory mechanisms in P-TEFb. Both mechanisms exert little effect on the P-TEFb-Tat interaction but prevent the P-TEFb-Tat complex from binding to TAR RNA. The first autoinhibition arises from the unphosphorylated state of Cdk9, which establishes a P-TEFb conformation unfavorable for TAR recognition. Autophosphorylation of Cdk9 overcomes this inhibition by inducing conformational changes in P-TEFb, thereby exposing a region in cyclin T1 for possible TAR binding. An intramolecular interaction between the N- and C-terminal regions of cyclin T1 sterically blocks the P-TEFb-TAR interaction and constitutes the second autoinhibitory mechanism. This inhibition is relieved by the binding of the C-terminal region of cyclin T1 to the transcription elongation factor Tat-SF1 and perhaps other cellular factors. Upon release from the intramolecular interaction, the C-terminal region also interacts with RNA polymerase II and is required for HIV-1 transcription, suggesting its role in bridging the P-TEFb-Tat-TAR complex and the basal elongation apparatus. These data reveal novel control mechanisms for the assembly of a multicomponent transcription elongation complex at the HIV-1 promoter.
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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.