Evidence map›Paper›PMID 28677507›Full record

ReviewCurrent pharmaceutical design2017

The HIV-1 Tat Protein: Mechanism of Action and Target for HIV-1 Cure Strategies.

Andrew P Rice

Open access · greenAbstract readReview
In one paragraph

Review in Current pharmaceutical design, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

67 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Testis Is a Sanctuary Site for HIV-1.Advances in experimental medicine and biology · 2025
    Review
  6. Article
  7. Article
  8. Article
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  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Andrew P RiceDepartment of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 77030. United States.
Baylor College of Medicine · US

Funding

Virology CoreP30AI036211 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BUTEL, JANET S · 1994 to 2015
$21.7M
Role of P-TEFB in HIV latencyR21AI116173 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI RICE, ANDREW P · 2014 to 2015
$435k
NIAID NIH HHS P30 AI036211NIAID NIH HHS R21 AI116173
6 · The paper itself

Abstract

The general mechanism involved in Tat activation of RNA Polymerase II (RNAP II) elongation of the integrated HIV-1 was elucidated over 20 years ago. This mechanism involves Tat binding to the TAR RNA element that forms at the 5' end of viral transcripts and recruiting a general RNAP II elongation factor termed as PTEFb. This elongation factor consists of CDK9 and Cyclin T1, and when recruited by Tat to TAR RNA, CDK9 was proposed to phosphorylate the carboxyl terminal domain of RNAP II and thereby activate elongation. Research in the past two decades has shown that the mechanism of Tat action is considerably more complicated than this simple model. In metabolically active cells, CDK9 and Cyclin T1 are now known to be largely sequestered in a RNA-protein complex termed the 7SK RNP. CDK9 and Cyclin T1 are released from the 7SK RNP by mechanisms not yet fully elucidated and along with Tat, bind to TAR RNA and orchestrate the assembly of a Super Elongation Complex (SEC) containing several additional proteins. CDK9 in the SEC then phosphorylates multiple substrates in the RNAP II complex to activate elongation. Importantly for therapeutic strategies, CDK9 and Cyclin T1 functions are down-regulated in resting CD4+ T cells that harbor latent HIV-1, and their up-regulation is required for reactivation of latent virus. Current strategies for a functional cure of HIV-1 infection therefore are likely to require development of latency reversal agents that up-regulate CDK9 and Cyclin T1 function in resting CD4+ T cells.

Indexed as

Anti-HIV AgentsCD4-Positive T-LymphocytesCyclin-Dependent Kinase 9Cyclin TDown-RegulationDrug DesignGene Expression Regulation, ViralHIV-1HIV InfectionsHumansRNA Polymerase IItat Gene Products, Human Immunodeficiency VirusUp-RegulationVirus LatencyAnti-HIV AgentsCyclin-Dependent Kinase 9Cyclin TRNA Polymerase IItat Gene Products, Human Immunodeficiency VirusCDK9Cyclin T1HIV-1HIV latencyP-TEFbTat

Identifiers

PMID28677507
PMCPMC5700838
OpenAlexW2735881021

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.