Evidence map›Paper›PMID 10888618›Full record

ArticleJournal of virology2000

The human factors YY1 and LSF repress the human immunodeficiency virus type 1 long terminal repeat via recruitment of histone deacetylase 1.

J J Coull, F Romerio, J M Sun, J L Volker, K M Galvin, J R Davie, Y Shi, U Hansen, D M Margolis

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02707900 (IGHID 11424 - A Pilot Trial of the Effect of Vorinostat and AGS-004 on Persistent HIV-1 Infection), which is not on this map. Cited by 216 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
216citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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.

NCT02707900 phase1terminatednot on this mapstarted 2016, after this paper: background citation

IGHID 11424 - A Pilot Trial of the Effect of Vorinostat and AGS-004 on Persistent HIV-1 Infection (The VOR VAX Study)

TypeinterventionalSponsorUniversity of North Carolina, Chapel HillRan2016 to 2018Enrolled6ConditionsHIV-1 InfectionArmsVorinostat, AGS-004
3 · Its place in the literature

Who cites it

216 citing papers in PubMed, 1 synthesis or guideline pooled it, 346 citations in OpenAlex.

  1. Pooled it
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  13. Article
  14. Targeting the PHF8/YY1 axis suppresses cancer cell growth through modulation of ROS.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Article
  16. HIV-1 Transcription Inhibition Using Small RNA-Binding Molecules.Pharmaceuticals (Basel, Switzerland) · 2023
    Article
  17. Review
  18. Review
  19. Article
  20. Review

156 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

9 authors at 5 institutions in 2 countries.

J J CoullDivision of Infectious Diseases, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9113, USA.
F Romerio
J M Sun
J L Volker
K M Galvin
J R Davie
Y Shi
U Hansen
D M Margolis
Harvard University · USThe University of Texas Southwestern Medical Center · USUniversity of Manitoba · CABiotechnology Institute · USDana-Farber Cancer Institute · US

Funding

TRANSCRIPTIONAL REPRESSION AND ACTIVATION BY YY1R01GM053874 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI SHI, YANG · 1996 to 2010
$4.6M
REPRESSION OF HIV TRANSCRIPTION--A PATHWAY TO QUIESCENCER01AI045297 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MARGOLIS, DAVID M. · 1999 to 2006
$2.5M
Repression of HIV Transcription: from mechanism to anti-latency therapiesR56AI045297 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MARGOLIS, DAVID M. · 2007 to 2007
$329k
HIV TRANSCRIPTIONAL REPRESSION--MECHANISM AND REGULATIONR21AI041366 · NIAID · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI MARGOLIS, DAVID M. · 1998 to 1999
–
NIAID NIH HHS AI 41366NIAID NIH HHS AI 45297NIAID NIH HHS R01 AI045297NIAID NIH HHS R56 AI045297NIGMS NIH HHS GM53874NIGMS NIH HHS R01 GM053874
6 · The paper itself

Abstract

Enigmatic mechanisms restore the resting state in activated lymphocytes following human immunodeficiency virus type 1 (HIV-1) infection, rarely allowing persistent nonproductive infection. We detail a mechanism whereby cellular factors could establish virological latency. The transcription factors YY1 and LSF cooperate in repression of transcription from the HIV-1 long terminal repeat (LTR). LSF recruits YY1 to the LTR via the zinc fingers of YY1. The first two zinc fingers were observed to be sufficient for this interaction in vitro. A mutant of LSF incapable of binding DNA blocked repression. Like other transcriptional repressors, YY1 can function via recruitment of histone deacetylase (HDAC). We find that HDAC1 copurifies with the LTR-binding YY1-LSF repressor complex, the domain of YY1 that interacts with HDAC1 is required to repress the HIV-1 promoter, expression of HDAC1 augments repression of the LTR by YY1, and the deacetylase inhibitor trichostatin A blocks repression mediated by YY1. This novel link between HDAC recruitment and inhibition of HIV-1 expression by YY1 and LSF, in the natural context of a viral promoter integrated into chromosomal DNA, is the first demonstration of a molecular mechanism of repression of HIV-1. YY1 and LSF may establish transcriptional and virological latency of HIV, a state that has recently been recognized in vivo and has significant implications for the long-term treatment of AIDS.

Indexed as

Gene Expression Regulation, ViralHIV Long Terminal RepeatDNA-Binding ProteinsDNA, ViralErythroid-Specific DNA-Binding FactorsHeLa CellsHistone DeacetylasesHIV-1HumansPromoter Regions, GeneticRNA-Binding ProteinsTranscription FactorsTranscription, GeneticVirionYY1 Transcription FactorDNA-Binding ProteinsDNA, ViralErythroid-Specific DNA-Binding FactorsHistone DeacetylasesRNA-Binding ProteinsTFCP2 protein, humanTranscription FactorsYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID10888618
PMCPMC112196
OpenAlexW2001356550

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.