ArticleBiology2012
Making a Short Story Long: Regulation of P-TEFb and HIV-1 Transcriptional Elongation in CD4+ T Lymphocytes and Macrophages.
Article in Biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- HIV-producing resting T cells monopolize virus production, associated PANoptosis, and persistence in lymphoid tissue.bioRxiv : the preprint server for biology · 2026Article
- ISG15-LFA1 interactions in latent HIV clearance: mechanistic implications in designing antiviral therapies.Frontiers in cell and developmental biology · 2024Article
- Initial productive and latent HIV infections originate in vivo by infection of resting T cells.The Journal of clinical investigation · 2023Article
- P-TEFb: The master regulator of transcription elongation.Molecular cell · 2023Review
- Heterogeneity of Latency Establishment in the Different Human CD4Journal of virology · 2022Article
- Functional impact of HIV-1 Tat on cells of the CNS and its role in HAND.Cellular and molecular life sciences : CMLS · 2020Review
- Underlying mechanisms of HIV-1 latency.Virus genes · 2017Review
- A mutant Tat protein inhibits infection of human cells by strains from diverse HIV-1 subtypes.Virology journal · 2017Article
- The MHC-II transactivator CIITA inhibits Tat function and HIV-1 replication in human myeloid cells.Journal of translational medicine · 2016Article
- Visualization of positive transcription elongation factor b (P-TEFb) activation in living cells.The Journal of biological chemistry · 2015Article
- Interaction between Tat and Drugs of Abuse during HIV-1 Infection and Central Nervous System Disease.Frontiers in microbiology · 2015Review
- A gene-specific role for the Ssu72 RNAPII CTD phosphatase in HIV-1 Tat transactivation.Genes & development · 2014Article
- Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Productive transcription of the integrated HIV-1 provirus is restricted by cellular factors that inhibit RNA polymerase II elongation. The viral Tat protein overcomes this by recruiting a general elongation factor, P-TEFb, to the TAR RNA element that forms at the 5' end of nascent viral transcripts. P-TEFb exists in multiple complexes in cells, and its core consists of a kinase, Cdk9, and a regulatory subunit, either Cyclin T1 or Cyclin T2. Tat binds directly to Cyclin T1 and thereby targets the Cyclin T1/P-TEFb complex that phosphorylates the CTD of RNA polymerase II and the negative factors that inhibit elongation, resulting in efficient transcriptional elongation. P-TEFb is tightly regulated in cells infected by HIV-1-CD4+ T lymphocytes and monocytes/macrophages. A number of mechanisms have been identified that inhibit P-TEFb in resting CD4+ T lymphocytes and monocytes, including miRNAs that repress Cyclin T1 protein expression and dephosphorylation of residue Thr186 in the Cdk9 T-loop. These repressive mechanisms are overcome upon T cell activation and macrophage differentiation when the permissivity for HIV-1 replication is greatly increased. This review will summarize what is currently known about mechanisms that regulate P-TEFb and how this regulation impacts HIV-1 replication and latency.
Identifiers
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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.