Evidence map›Paper›PMID 27110708›Full record

ArticleVirology2016

Methylation status and AP1 elements are involved in EBV-mediated miR-155 expression in EBV positive lymphoma cells.

Qinyan Yin, Xia Wang, Claire Roberts, Erik K Flemington, Joseph A Lasky

Open access · greenAbstract read
In one paragraph

Article in Virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Viral miRNA regulation of host gene expression.Seminars in cell & developmental biology · 2023
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Viruses and miRNAs: More Friends than Foes.Frontiers in microbiology · 2017
    Review
  9. Article
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

5 authors at 1 institution in 1 country.

Qinyan YinSection of Pulmonary Diseases, Critical Care and Environmental Medicine, Department of Medicine, SL9, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA. Electronic address: qyin@tulane.edu.
Xia WangDepartment of Pathology and Laboratory Medicine, SL79, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA. Electronic address: xwang4@tulane.edu.
Claire RobertsDepartment of Pathology and Laboratory Medicine, SL79, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA. Electronic address: cfewell@tulane.edu.
Erik K FlemingtonDepartment of Pathology and Laboratory Medicine, SL79, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA. Electronic address: erik@tulane.edu.
Joseph A LaskySection of Pulmonary Diseases, Critical Care and Environmental Medicine, Department of Medicine, SL9, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA. Electronic address: jlasky@tulane.edu.
Tulane University · US

Funding

Epstein Barr virus antisense transcriptionR01AI106676 · NIAID · TULANE UNIVERSITY OF LOUISIANA · PI FLEMINGTON, ERIK K · 2014 to 2018
$1.9M
Intercellular communication in Epstein Barr virus reactivationR01AI101046 · NIAID · TULANE UNIVERSITY OF LOUISIANA · PI FLEMINGTON, ERIK K · 2012 to 2016
$1.9M
Training in Lung Molecular and Cell Pathobiology-Phase IIT32HL007973 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI LASKY, JOSEPH A · 2003 to 2013
$1.5M
NHLBI NIH HHS T32 HL007973NIAID NIH HHS R01 AI101046NIAID NIH HHS R01 AI106676
6 · The paper itself

Abstract

The relationship between Epstein Barr Virus (EBV) and miR-155 is well established. EBV infection induces miR-155 expression, which is expressed at higher levels in EBV latency type III cells compared to EBV latency type I cells. However, the mechanism by which EBV latency genes activate miR-155 expression is still unclear. Here we present data showing that DNA methylation regulates miR-155 expression. We also provide evidence that the AP1 signaling pathway is involved in EBV-mediated miR-155 activation, and that Bay11 influences signaling of the miR-155 promoter AP1 element. Lastly, we show that LMP2A, LMP1 and EBNAs cannot activate miR-155 expression alone, indicating that the regulation of miR-155 by EBV is dependent on more than one EBV gene or cell signaling pathway. We conclude that the regulation of miR-155 in EBV-positive cells occurs through multiple cell signaling processes involving EBV-mediated chromatin remodeling, cell signaling regulation and transcription factor activation.

Indexed as

DNA MethylationResponse ElementsBase SequenceBinding SitesCell LineCpG IslandsEpstein-Barr Virus InfectionsEpstein-Barr Virus Nuclear AntigensGene Expression RegulationHerpesvirus 4, HumanHumansLymphomaMicroRNAsModels, BiologicalPromoter Regions, GeneticProtein BindingEpstein-Barr Virus Nuclear AntigensMicroRNAsMIRN155 microRNA, humanTranscription Factor AP-1AP1DNA methylationEBNAsEBVEpstein Barr VirusLMPsMicroRNAMiR-155MiRNAPri-miR-155

Identifiers

PMID27110708
PMCPMC4884481
OpenAlexW2343221374

What OpenQuestion holds

Textmetadata
LicenceTDM
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.