Evidence map›Paper›PMID 21994798›Full record

ReviewViruses2011

Unconventional use of LC3 by coronaviruses through the alleged subversion of the ERAD tuning pathway.

Fulvio Reggiori, Cornelis A M de Haan, Maurizio Molinari

Abstract readReview
In one paragraph

Review in Viruses, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

17 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  9. Inhibitors of VPS34 and lipid metabolism suppress SARS-CoV-2 replication.bioRxiv : the preprint server for biology · 2020
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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

3 authors.

Fulvio ReggioriDepartment of Cell Biology and Institute of Biomembranes, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands. F.Reggiori@umcutrecht.nl
Cornelis A M de Haan
Maurizio Molinari

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathogens of bacterial and viral origin hijack pathways operating in eukaryotic cells in many ways in order to gain access into the host, to establish themselves and to eventually produce their progeny. The detailed molecular characterization of the subversion mechanisms devised by pathogens to infect host cells is crucial to generate targets for therapeutic intervention. Here we review recent data indicating that coronaviruses probably co-opt membranous carriers derived from the endoplasmic reticulum, which contain proteins that regulate disposal of misfolded polypeptides, for their replication. In addition, we also present models describing potential mechanisms that coronaviruses could employ for this hijacking.

Indexed as

Endoplasmic Reticulum-Associated DegradationVirus ReplicationAnimalsAutophagyCoronaviridaeCoronaviridae InfectionsEndoplasmic ReticulumHumansMammalsMembrane ProteinsMiceMicrotubule-Associated ProteinsModels, BiologicalTransport VesiclesMAP1LC3A protein, humanMembrane ProteinsMicrotubule-Associated Proteinsautophagycoronavirusesdouble-membrane vesiclesEDEM1EDEMosomesERADER quality controlMHVnidovirusesOS-9SARS-coronavirus

Identifiers

PMID21994798
PMCPMC3187687

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.