ArticleMolecular and cellular biology2004
A human immunodeficiency virus type 1 Tat-like arginine-rich RNA-binding domain is essential for HEXIM1 to inhibit RNA polymerase II transcription through 7SK snRNA-mediated inactivation of P-TEFb.
Article in Molecular and cellular biology, 2004. 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, 124 citations in OpenAlex.
- HEXIM1 inter-monomer autoinhibition governs 7SK RNA binding specificity and P-TEFb inactivation.Nature communications · 2026Article
- The HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- Bioinformatics Insights on Viral Gene Expression Transactivation: From HIV-1 to SARS-CoV-2.International journal of molecular sciences · 2024Article
- Catalytic activity of the Bin3/MePCE methyltransferase domain is dispensable for 7SK snRNP function in Drosophila melanogaster.Genetics · 2024Article
- Progress in 7SK ribonucleoprotein structural biology.Frontiers in molecular biosciences · 2023Review
- Identification of Novel Nucleocapsid Chimeric Proteins Inhibiting HIV-1 Replication.International journal of molecular sciences · 2022Article
- A structure-based mechanism for displacement of the HEXIM adapter from 7SK small nuclear RNA.Communications biology · 2022Article
- Tip110 Expression Facilitates the Release of HEXIM1 and pTEFb from the 7SK Ribonucleoprotein Complex Involving Regulation of the Intracellular Redox Level.Aging and disease · 2021Article
- Combinatorial Use of Both Epigenetic and Non-Epigenetic Mechanisms to Efficiently Reactivate HIV Latency.International journal of molecular sciences · 2021Review
- Review
- Different views of the dynamic landscape covered by the 5'-hairpin of the 7SK small nuclear RNA.RNA (New York, N.Y.) · 2020Article
- Review
- P-TEFb as A Promising Therapeutic Target.Molecules (Basel, Switzerland) · 2020Review
- Structural transitions in the RNA 7SK 5' hairpin and their effect on HEXIM binding.Nucleic acids research · 2020Article
- From Entry to Egress: Strategic Exploitation of the Cellular Processes by HIV-1.Frontiers in microbiology · 2020Review
- Article
- HEXIM1-Tat chimera inhibits HIV-1 replication.PLoS pathogens · 2018Article
- HIV-1 Tat interactions with cellular 7SK and viral TAR RNAs identifies dual structural mimicry.Nature communications · 2018Article
- Article
- Hexim1, an RNA-controlled protein hub.Transcription · 2018Review
10 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
The HEXIM1 protein inhibits the kinase activity of P-TEFb (CDK9/cyclin T) to suppress RNA polymerase II transcriptional elongation in a process that specifically requires the 7SK snRNA, which mediates the interaction of HEXIM1 with P-TEFb. In an attempt to define the sequence requirements for HEXIM1 to interact with 7SK and inactivate P-TEFb, we have identified the first 18 amino acids within the previously described nuclear localization signal (NLS) of HEXIM1 as both necessary and sufficient for binding to 7SK in vivo and in vitro. This 7SK-binding motif was essential for HEXIM1's inhibitory action, as the HEXIM1 mutants with this motif replaced with a foreign NLS failed to interact with 7SK and P-TEFb and hence were unable to inactivate P-TEFb. The 7SK-binding motif alone, however, was not sufficient to inhibit P-TEFb. A region C-terminal to this motif was also required for HEXIM1 to associate with P-TEFb and suppress P-TEFb's kinase and transcriptional activities. The 7SK-binding motif in HEXIM1 contains clusters of positively charged residues reminiscent of the arginine-rich RNA-binding motif found in a wide variety of proteins. Part of it is highly homologous to the TAR RNA-binding motif in the human immunodeficiency virus type 1 (HIV-1) Tat protein, which was able to restore the 7SK-binding ability of a HEXIM1 NLS substitution mutant. We propose that a similar RNA-protein recognition mechanism may exist to regulate the formation of both the Tat-TAR-P-TEFb and the HEXIM1-7SK-P-TEFb ternary complexes, which may help convert the inactive HEXIM1/7SK-bound P-TEFb into an active one for Tat-activated and TAR-dependent HIV-1 transcription.
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