Evidence map›Paper›PMID 29354130›Full record

ArticleFrontiers in immunology2017

Ets-2 Acts As a Transcriptional Repressor of the Human Immunodeficiency Virus Type 1 through Binding to a Repressor-Activator Target Sequence of 5'-LTR.

Ioannis Panagoulias, Fotios Karagiannis, Ioanna Aggeletopoulou, Tassos Georgakopoulos, Christos P Argyropoulos, Karolina Akinosoglou, Charalambos Gogos, Athanasios Skoutelis, Athanasia Mouzaki

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 47% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

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  8. Barriers for HIV Cure: The Latent Reservoir.AIDS research and human retroviruses · 2018
    Review
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 4 institutions in 2 countries.

Ioannis PanagouliasDivision of Hematology, Department of Internal Medicine, Medical School, University of Patras, Patras, Greece.
Fotios KaragiannisDivision of Hematology, Department of Internal Medicine, Medical School, University of Patras, Patras, Greece.
Ioanna AggeletopoulouDivision of Hematology, Department of Internal Medicine, Medical School, University of Patras, Patras, Greece.
Tassos GeorgakopoulosDivision of Hematology, Department of Internal Medicine, Medical School, University of Patras, Patras, Greece.
Christos P ArgyropoulosDivision of Nephrology, Department of Internal Medicine, Medical School, University of New Mexico, Albuquerque, NM, United States.
Karolina AkinosoglouInfectious Diseases Unit, Department of Internal Medicine, University Hospital of Patras, Patras, Greece.
Charalambos GogosInfectious Diseases Unit, Department of Internal Medicine, University Hospital of Patras, Patras, Greece.
Athanasios SkoutelisDepartment of Internal Medicine and Infectious Diseases Unit, Evangelismos General Hospital, Athens, Greece.
Athanasia MouzakiDivision of Hematology, Department of Internal Medicine, Medical School, University of Patras, Patras, Greece.
University of Patras · GRGeneral University Hospital of Patras · GREvangelismos Hospital · GRUniversity of New Mexico · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIV-1 is transcriptionally active in activated T helper (Th)-cells and inactive in naive or resting memory Th-cells. Ets-2 is a preinduction transcriptional repressor of the IL-2 gene in naive Th-cells and a candidate transcriptional repressor of HIV-1 in the same cells, because the -279 to -250 upstream region of HIV-1-LTR [repressor-activator target sequence (RATS)], that participates in HIV-1-LTR transcriptional silencing, encompasses the AAGGAG Ets-2 binding site. In this proof of concept study, we investigated whether Ets-2 represses the expression of HIV-1. To assess whether Ets-2 can repress HIV-1 transcriptional activation acting through RATS, we transfected Jurkat cells with an Ets-2 overexpression plasmid (pCDNA3-ets-2) or Ets-2 silencing plasmids (ets-2-shRNA) and, as target genes, plasmids carrying the whole HIV-1-LTR sequence (HIV-1-LTR-CAT) or two copies of the RATS sequence (2× RATS-CAT) or a point mutation in the Ets-2 binding site (2× mutantRATS-CAT) or CMV-CAT (control). Ets-2 overexpression resulted in a significant reduction of HIV-1-LTR-CAT and 2× RATS-CAT activities in stimulated cells, but not of the 2× mutantRATS-CAT or CMV-CAT. Ets-2 silencing led to increased activities of HIV-1-LTR-CAT and 2× RATS-CAT in unstimulated cells, but had no effect on the activities of 2× mutantRATS-CAT and CMV-CAT. To assess Ets-2 binding to HIV-1-LTR-RATS in naive Th-cells, we isolated naive Th-cell nuclear proteins and passed them through an Ets-2 antibody column; electrophoretic mobility shift assays were performed using an RATS probe mixed with consecutive protein eluates. Ets-2 bound to the HIV-1-LTR-RATS in a dose-dependent manner. To assess Ets-2 binding to RATS

Indexed as

Ets-2HIV-1naive T cellsrepressorrepressor–activator target sequenceT helper cellstranscription factorsviral latency

Identifiers

PMID29354130
PMCPMC5758550
OpenAlexW2782350003

What OpenQuestion holds

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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.