ArticleRetrovirology2006
Phosphorylation of HIV-1 Tat by CDK2 in HIV-1 transcription.
Article in Retrovirology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 94 citations in OpenAlex.
- HIV associated immune aging among people living with HIV: implications for long-term antiretroviral therapy and potential HIV cure interventions in sub-Saharan Africa.Frontiers in immunology · 2026Review
- SARS-CoV-2 hijacks cellular kinase CDK2 to promote viral RNA synthesis.Signal transduction and targeted therapy · 2022Article
- When cyclin-dependent kinases meet viral infections, including SARS-CoV-2.Journal of medical virology · 2022Review
- HIV-1 infection in sickle cell disease and sickle cell trait: role of iron and innate response.Expert review of hematology · 2022Article
- Insights Into Persistent HIV-1 Infection and Functional Cure: Novel Capabilities and Strategies.Frontiers in microbiology · 2022Review
- Targeting Tat-TAR RNA Interaction for HIV-1 Inhibition.Viruses · 2021Article
- A Stronger Transcription Regulatory Circuit of HIV-1C Drives the Rapid Establishment of Latency with Implications for the Direct Involvement of Tat.Journal of virology · 2020Article
- Filgotinib suppresses HIV-1-driven gene transcription by inhibiting HIV-1 splicing and T cell activation.The Journal of clinical investigation · 2020Article
- Article
- Long Non-coding RNAs Mechanisms of Action in HIV-1 Modulation and the Identification of Novel Therapeutic Targets.Non-coding RNA · 2020Review
- Block-And-Lock Strategies to Cure HIV Infection.Viruses · 2020Review
- Specific ActivationJournal of virology · 2019Article
- Effect of transcription inhibition and generation of suppressive viral non-coding RNAs.Retrovirology · 2019Article
- Roles of CDKs in RNA polymerase II transcription of the HIV-1 genome.Transcription · 2019Review
- Genetic variation and function of the HIV-1 Tat protein.Medical microbiology and immunology · 2019Review
- Article
- HIV-1 Tat phosphorylation on Ser-16 residue modulates HIV-1 transcription.Retrovirology · 2018Article
- Post-translational Modification-Based Regulation of HIV Replication.Frontiers in microbiology · 2018Review
- Grass Carp Reovirus VP41 Targets Fish MITA To Abrogate the Interferon Response.Journal of virology · 2017Article
- Increased iron export by ferroportin induces restriction of HIV-1 infection in sickle cell disease.Blood advances · 2016Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundTranscription of HIV-1 genes is activated by HIV-1 Tat protein, which induces phosphorylation of RNA polymerase II (RNAPII) C-terminal domain (CTD) by CDK9/cyclin T1. Earlier we showed that CDK2/cyclin E phosphorylates HIV-1 Tat in vitro. We also showed that CDK2 induces HIV-1 transcription in vitro and that inhibition of CDK2 expression by RNA interference inhibits HIV-1 transcription and viral replication in cultured cells. In the present study, we analyzed whether Tat is phosphorylated in cultured cells by CDK2 and whether Tat phosphorylation has a regulatory effect on HIV-1 transcription.
resultsWe analyzed HIV-1 Tat phosphorylation by CDK2 in vitro and identified Ser16 and Ser46 residues of Tat as potential phosphorylation sites. Tat was phosphorylated in HeLa cells infected with Tat-expressing adenovirus and metabolically labeled with 32P. CDK2-specific siRNA reduced the amount and the activity of cellular CDK2 and significantly decreased phosphorylation of Tat. Tat co-migrated with CDK2 on glycerol gradient and co-immunoprecipitated with CDK2 from the cellular extracts. Tat was phosphorylated on serine residues in vivo, and mutations of Ser16 and Ser46 residues of Tat reduced Tat phosphorylation in vivo. Mutation of Ser16 and Ser46 residues of Tat reduced HIV-1 transcription in transiently transfected cells. The mutations of Tat also inhibited HIV-1 viral replication and Tat phosphorylation in the context of the integrated HIV-1 provirus. Analysis of physiological importance of the S16QP(K/R)19 and S46YGR49 sequences of Tat showed that Ser16 and Ser46 and R49 residues are highly conserved whereas mutation of the (K/R)19 residue correlated with non-progression of HIV-1 disease.
conclusionOur results indicate for the first time that Tat is phosphorylated in vivo; Tat phosphorylation is likely to be mediated by CDK2; and phosphorylation of Tat is important for HIV-1 transcription.
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