Evidence map›Paper›PMID 18007589›Full record

ArticleThe EMBO journal2007

CBF-1 promotes transcriptional silencing during the establishment of HIV-1 latency.

Mudit Tyagi, Jonathan Karn

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2007. 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 156 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% 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

156 citing papers in PubMed, 1 synthesis or guideline pooled it, 217 citations in OpenAlex.

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96 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

2 authors at 1 institution in 1 country.

Mudit TyagiDepartment of Molecular Biology and Microbiology, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.
Jonathan Karn
Case Western Reserve University · US

Funding

WG3: HIV, Co-infections and Co-morbiditiesP30AI036219 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI Sharon L. Hillier, JONATHAN KARN · 1994 to 2026
$50.0M
Molecular mechanisms regulating HIV entry and exit from latencyR01AI067093 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI KARN, JONATHAN · 2007 to 2011
$1.9M
NIAID NIH HHS AI036219NIAID NIH HHS AI067093NIAID NIH HHS P30 AI036219NIAID NIH HHS R01 AI067093
6 · The paper itself

Abstract

The establishment of HIV proviral latency requires the creation of repressive chromatin structures that impair the initiation of transcription and restrict RNAP II elongation. We have found that C-promoter binding factor-1 (CBF-1), a CSL (CBF-1, Su(H) and Lag-1)-type transcription factor and key effector of the Notch signaling pathway, is a remarkably potent and specific inhibitor of the HIV-1 LTR promoter. Knockdown of endogenous CBF-1 using specific small hairpin RNAs expressed on lentiviral vectors results in the partial reactivation of latent HIV proviruses, recruitment of RNAP II, loss of histone deacetylases and the concomitant acetylation of histones. An important property of any repressor utilized to establish HIV latency is that it must become displaced or deactivated upon T-cell activation. Consistent with this hypothesis, CBF-1 mRNA and protein levels are highest in quiescent or unstimulated T cells but decline rapidly in response to proliferative stimulation such as activation of the T-cell receptor or treatment with TNF-alpha. We conclude that CBF-1 is a previously overlooked factor that induces transcriptional silencing during the establishment of HIV latency.

Indexed as

Gene Expression Regulation, ViralGene SilencingHIV-1Transcription, GeneticAnimalsBinding SitesChromatinGenetic VectorsHeLa CellsHistone DeacetylasesHIV InfectionsHIV Long Terminal RepeatHumansImmunoglobulin J Recombination Signal Sequence-Binding ProteinJurkat CellsLentivirusChromatinHistone DeacetylasesImmunoglobulin J Recombination Signal Sequence-Binding ProteinRecombinant Fusion ProteinsRNA

Identifiers

PMID18007589
PMCPMC2140115
OpenAlexW2102824612

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.