ArticleProteomics2015
Phosphorylation of HEXIM1 at Tyr271 and Tyr274 Promotes Release of P-TEFb from the 7SK snRNP Complex and Enhances Proviral HIV Gene Expression.
Article in Proteomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 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
20 citing papers in PubMed, 26 citations in OpenAlex.
- HEXIM1 inter-monomer autoinhibition governs 7SK RNA binding specificity and P-TEFb inactivation.Nature communications · 2026Article
- The cell biology of HIV-1 latency and rebound.Retrovirology · 2024Review
- Article
- New insights into transcription elongation control of HIV-1 latency and rebound.Trends in immunology · 2023Review
- Review
- Regulation of RNA polymerase II activity is essential for terminal erythroid maturation.Blood · 2021Article
- CDK9 keeps RNA polymerase II on track.Cellular and molecular life sciences : CMLS · 2021Review
- Dysregulation of Cell Signaling by SARS-CoV-2.Trends in microbiology · 2021Review
- Review
- Article
- P-TEFb as A Promising Therapeutic Target.Molecules (Basel, Switzerland) · 2020Review
- Activation of P-TEFb by cAMP-PKA signaling in autosomal dominant polycystic kidney disease.Science advances · 2019Article
- Cyclin-dependent kinase 7 (CDK7)-mediated phosphorylation of the CDK9 activation loop promotes P-TEFb assembly with Tat and proviral HIV reactivation.The Journal of biological chemistry · 2018Article
- Hexim1, an RNA-controlled protein hub.Transcription · 2018Review
- HIV signaling through CD4 and CCR5 activates Rho family GTPases that are required for optimal infection of primary CD4+ T cells.Retrovirology · 2017Article
- Role of Host Factors on the Regulation of Tat-Mediated HIV-1 Transcription.Current pharmaceutical design · 2017Review
- An evolutionary conserved Hexim1 peptide binds to the Cdk9 catalytic site to inhibit P-TEFb.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Cracking the control of RNA polymerase II elongation by 7SK snRNP and P-TEFb.Nucleic acids research · 2016Review
- Article
- Article
Corrections and comments
- Erratum issuedErrata.2016
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Efficient HIV transcription requires P-TEFb, an essential co-factor for Tat. In actively replicating cells, P-TEFb is incorporated into the 7SK snRNP complex together with the repressor protein HEXIM1. Using an affinity purification-tandem mass spectrometry approach to identify modification sites on HEXIM1 that regulate the sequestration of P-TEFb by 7SK snRNP, we found that HEXIM1 can be phosphorylated on adjacent residues in a region immediately upstream of the coiled-coil dimerization domain (Ser268, Thr270, Tyr271, and Tyr274). Phosphomimetic mutations of Tyr271 and Tyr274 disrupted the assembly of P-TEFb and HEXIM1 into the 7SK snRNP complex. Although Y271E/Y274E did not adversely affect the nuclear localization pattern of HEXIM1, it induced the redistribution of the CDK9 subunit of P-TEFb into the cytoplasm. By contrast, the Y271F/Y274F HEXIM1 mutant assembled normally with P-TEFb within the 7SK snRNP complex but severely reduced proviral gene expression in T cells in response to activation signals and caused a severe growth defect of Jurkat T cells. Thus, Y271F/Y274F, which cannot be phosphorylated on these residues, appears to block the exchange of active P-TEFb from the 7SK complex, thereby limiting the level of P-TEFb below the threshold required to support transcription elongation of the HIV provirus and cellular genes.
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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.