Evidence map›Paper›PMID 32332742›Full record

ArticleNature communications2020

The UPR sensor IRE1α and the adenovirus E3-19K glycoprotein sustain persistent and lytic infections.

Vibhu Prasad, Maarit Suomalainen, Yllza Jasiqi, Silvio Hemmi, Patrick Hearing, Louise Hosie, Hans-Gerhard Burgert, Urs F Greber

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Review
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  9. Article
  10. Dynamic modulation of IRE1α-XBP1 signaling by adenovirus.bioRxiv : the preprint server for biology · 2024
    Article
  11. Article
  12. Review
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  15. Article
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  18. Molecular Mechanism Underlying Role of the XBP1s in Cardiovascular Diseases.Journal of cardiovascular development and disease · 2022
    Review
  19. Article
  20. 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

8 authors at 4 institutions in 4 countries.

Vibhu PrasadDepartment of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.ORCID http://orcid.org/0000-0001-7450-607X
Maarit SuomalainenDepartment of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.ORCID http://orcid.org/0000-0002-3276-3008
Yllza JasiqiDepartment of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
Silvio HemmiDepartment of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
Patrick HearingDepartment of Molecular Genetics and Microbiology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY, USA.
Louise HosieUniversity of Warwick, School of Life Sciences, Coventry, CV4 7AL, UK.ORCID http://orcid.org/0000-0001-7298-4262
Hans-Gerhard BurgertUniversity of Warwick, School of Life Sciences, Coventry, CV4 7AL, UK.
Urs F GreberDepartment of Molecular Life Sciences, University of Zurich, Zurich, Switzerland. urs.greber@mls.uzh.ch.ORCID http://orcid.org/0000-0003-2278-120X
University of Zurich · CHStony Brook School · USThe Francis Crick Institute · GBUniversity Medical Center Freiburg · DE

Funding

Regulation of Nuclear Signaling Pathways by the Adenovirus E4-ORF3 ProteinR01CA122677 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI HEARING, PATRICK · 2007 to 2022
$5.2M
NCI NIH HHS R01 CA122677
6 · The paper itself

Abstract

Persistent viruses cause chronic disease, and threaten the lives of immunosuppressed individuals. Here, we elucidate a mechanism supporting the persistence of human adenovirus (AdV), a virus that can kill immunosuppressed patients. Cell biological analyses, genetics and chemical interference demonstrate that one of five AdV membrane proteins, the E3-19K glycoprotein specifically triggers the unfolded protein response (UPR) sensor IRE1α in the endoplasmic reticulum (ER), but not other UPR sensors, such as protein kinase R-like ER kinase (PERK) and activating transcription factor 6 (ATF6). The E3-19K lumenal domain activates the IRE1α nuclease, which initiates mRNA splicing of X-box binding protein-1 (XBP1). XBP1s binds to the viral E1A-enhancer/promoter sequence, and boosts E1A transcription, E3-19K levels and lytic infection. Inhibition of IRE1α nuclease interrupts the five components feedforward loop, E1A, E3-19K, IRE1α, XBP1s, E1A enhancer/promoter. This loop sustains persistent infection in the presence of the immune activator interferon, and lytic infection in the absence of interferon.

Indexed as

A549 CellsAdenoviridaeAdenoviridae InfectionsAdenovirus E1A ProteinsAdenovirus E3 ProteinsChronic DiseaseEndoplasmic ReticulumEndoribonucleasesGene Expression Regulation, ViralGene Knockdown TechniquesGene Knockout TechniquesHeLa CellsHost-Pathogen InteractionsHumansImmunocompromised HostInterferon-gammaAdenovirus E1A ProteinsAdenovirus E3 ProteinsEndoribonucleasesERN1 protein, humanIFNG protein, humanInterferon-gammaProtein Serine-Threonine KinasesX-Box Binding Protein 1XBP1 protein, human

Identifiers

PMID32332742
PMCPMC7181865
OpenAlexW3017712133

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.