ReviewBiochemical Society transactions2020
ER functions are exploited by viruses to support distinct stages of their life cycle.
Review in Biochemical Society transactions, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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.
Who cites it
15 citing papers in PubMed.
- PRRSV suppresses ER-phagy through Nsp2- and Nsp5-mediated degradation of FAM134B.Frontiers in cellular and infection microbiology · 2026Article
- Cholesterol sensing by the SCAP-FAM134B complex regulates ER-phagy and STING innate immunity.Nature cell biology · 2025Article
- The Japanese encephalitis virus NS1 protein concentrates ER membranes in a cytoskeleton-independent manner to facilitate viral replication.Journal of virology · 2025Article
- PRRSV non-structural protein 5 inhibits antiviral innate immunity by degrading multiple proteins of RLR signaling pathway through FAM134B-mediated ER-phagy.Journal of virology · 2024Article
- The astrovirus N-terminal nonstructural protein anchors replication complexes to the perinuclear ER membranes.PLoS pathogens · 2024Article
- The endoplasmic reticulum (ER): a crucial cellular hub in flavivirus infection and potential target site for antiviral interventions.Npj viruses · 2024Review
- Autophagy of the ER: the secretome finds the lysosome.The FEBS journal · 2023Review
- The REEP5/TRAM1 complex binds SARS-CoV-2 NSP3 and promotes virus replication.Journal of virology · 2023Article
- Cellular Stress: Modulator of Regulated Cell Death.Biology · 2023Review
- Reticulons promote formation of ER-derived double-membrane vesicles that facilitate SARS-CoV-2 replication.The Journal of cell biology · 2023Article
- Article
- A specific EMC subunit supports Dengue virus infection by promoting virus membrane fusion essential for cytosolic genome delivery.PLoS pathogens · 2022Article
- Know your enemy and know yourself - the case of SARS-CoV-2 host factors.Current opinion in virology · 2021Review
- RNA-Binding Proteins at the Host-Pathogen Interface Targeting Viral Regulatory Elements.Viruses · 2021Article
- ER-Phagy and Microbial Infection.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The endoplasmic reticulum (ER), with its expansive membranous system and a vast network of chaperones, enzymes, sensors, and ion channels, orchestrates diverse cellular functions, ranging from protein synthesis, folding, secretion, and degradation to lipid biogenesis and calcium homeostasis. Strikingly, some of the functions of the ER are exploited by viruses to promote their life cycles. During entry, viruses must penetrate a host membrane and reach an intracellular destination to express and replicate their genomes. These events lead to the assembly of new viral progenies that exit the host cell, thereby initiating further rounds of infection. In this review, we highlight how three distinct viruses - polyomavirus, flavivirus, and coronavirus - co-opt key functions of the ER to cause infection. We anticipate that illuminating this virus-ER interplay will provide rational therapeutic approaches to combat the virus-induced diseases.
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Registered trials
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.