Evidence map›Paper›PMID 31733451›Full record

ArticleVirology2020

EGR1 upregulation following Venezuelan equine encephalitis virus infection is regulated by ERK and PERK pathways contributing to cell death.

Bibha Dahal, Shih-Chao Lin, Brian D Carey, Jonathan L Jacobs, Jonathan D Dinman, Monique L van Hoek, Andre A Adams, Kylene Kehn-Hall

Open access · bronzeAbstract read
In one paragraph

Article in Virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.1field-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.

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

16 citing papers in PubMed, 28 citations in OpenAlex.

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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

8 authors at 4 institutions in 2 countries.

Bibha DahalNational Center for Biodefense and Infectious Diseases, School of Systems Biology, George Mason University, Manassas, VA, USA.
Shih-Chao LinNational Center for Biodefense and Infectious Diseases, School of Systems Biology, George Mason University, Manassas, VA, USA.
Brian D CareyNational Center for Biodefense and Infectious Diseases, School of Systems Biology, George Mason University, Manassas, VA, USA.
Jonathan L JacobsQIAGEN Bioinformatics, Aarhus, Denmark; QIAGEN Bioinformatics, Maryland, USA.
Jonathan D DinmanDepartment of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD, USA.
Monique L van HoekNational Center for Biodefense and Infectious Diseases, School of Systems Biology, George Mason University, Manassas, VA, USA.
Andre A AdamsNaval Research Laboratory, Washington, DC, USA.
Kylene Kehn-HallNational Center for Biodefense and Infectious Diseases, School of Systems Biology, George Mason University, Manassas, VA, USA. Electronic address: kkehnhal@gmu.edu.
George Mason University · USQiagen (Denmark) · DKUnited States Naval Research Laboratory · USUniversity of Maryland, College Park · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Venezuelan equine encephalitis virus (VEEV) is a neurotropic virus that causes significant disease in both humans and equines. Here we characterized the impact of VEEV on signaling pathways regulating cell death in human primary astrocytes. VEEV productively infected primary astrocytes and caused an upregulation of early growth response 1 (EGR1) gene expression at 9 and 18 h post infection. EGR1 induction was dependent on extracellular signal-regulated kinase1/2 (ERK1/2) and protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), but not on p38 mitogen activated protein kinase (MAPK) or phosphoinositide 3-kinase (PI3K) signaling. Knockdown of EGR1 significantly reduced VEEV-induced apoptosis and impacted viral replication. Knockdown of ERK1/2 or PERK significantly reduced EGR1 gene expression, dramatically reduced viral replication, and increased cell survival as well as rescued cells from VEEV-induced apoptosis. These data indicate that EGR1 activation and subsequent cell death are regulated through ERK and PERK pathways in VEEV infected primary astrocytes.

Indexed as

Cell DeathApoptosisAstrocytesCells, CulturedCell SurvivalEarly Growth Response Protein 1eIF-2 KinaseEncephalitis Virus, Venezuelan EquineEncephalomyelitis, Venezuelan EquineGene ExpressionGene Knockdown TechniquesHumansMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Signal TransductionVirus ReplicationEarly Growth Response Protein 1EGR1 protein, humanEIF2AK3 protein, humaneIF-2 KinaseMAPK1 protein, humanMAPK3 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3AlphavirusApoptosisEarly growth response 1EGR1ERKPERKUnfolded protein responseUPRVEEVVenezuelan equine encephalitis virus

Identifiers

PMID31733451
PMCPMC7126400
OpenAlexW2983546016

What OpenQuestion holds

Textmetadata
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.