ReviewJournal of virology2014
How viruses hijack the ERAD tuning machinery.
Review in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 26 papers.
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.
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
26 citing papers in PubMed, 43 citations in OpenAlex.
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- Viruses and autophagy: bend, but don't break.Nature reviews. Microbiology · 2024Review
- Is cholesterol both the lock and key to abnormal transmembrane signals in Autism Spectrum Disorder?Lipids in health and disease · 2024Article
- Protein Quality Control Systems and ER Stress as Key Players in SARS-CoV-2-Induced Neurodegeneration.Cells · 2024Review
- ELM-the Eukaryotic Linear Motif resource-2024 update.Nucleic acids research · 2024Article
- Gold nanoparticles combat enveloped RNA virus by affecting organelle dynamics.Signal transduction and targeted therapy · 2023Article
- HuCoPIA: An Atlas of Human vs. SARS-CoV-2 Interactome and the Comparative Analysis with OtherViruses · 2023Article
- Endomembrane remodeling in SARS-CoV-2 infection.Cell insight · 2022Review
- The interplay between pathogens and Atg8 family proteins: thousand-faced interactions.FEBS open bio · 2021Review
- Multi-level inhibition of coronavirus replication by chemical ER stress.Nature communications · 2021Article
- Review
- Flavivirus Replication Organelle Biogenesis in the Endoplasmic Reticulum: Comparison with Other Single-Stranded Positive-Sense RNA Viruses.International journal of molecular sciences · 2019Review
- Host Gene SEL1L Involved in Endoplasmic Reticulum-Associated Degradation Pathway Could Inhibit Hepatitis B Virus at RNA, DNA, and Protein Levels.Frontiers in microbiology · 2019Article
- Estrogens Promote Misfolded Proinsulin Degradation to Protect Insulin Production and Delay Diabetes.Cell reports · 2018Article
- Innate Sensing of Influenza A Virus Hemagglutinin Glycoproteins by the Host Endoplasmic Reticulum (ER) Stress Pathway Triggers a Potent Antiviral Response via ER-Associated Protein Degradation.Journal of virology · 2018Article
- Article
- Article
- TRPM7 senses oxidative stress to release ZnProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Reliance ofGenetics · 2017Article
- Review
Corrections and comments
- Correction · 2015-04-01Cites Retracted Work · Error in Image · Error in Text ·
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An essential step during the intracellular life cycle of many positive-strand RNA viruses is the rearrangement of host cell membranes to generate membrane-bound replication platforms. For example, Nidovirales and Flaviviridae subvert the membrane of the endoplasmic reticulum (ER) for their replication. However, the absence of conventional ER and secretory pathway markers in virus-induced ER-derived membranes has for a long time hampered a thorough understanding of their biogenesis. Recent reports highlight the analogies between mouse hepatitis virus-, equine arteritis virus-, and Japanese encephalitis virus-induced replication platforms and ER-associated degradation (ERAD) tuning vesicles (or EDEMosomes) that display nonlipidated LC3 at their cytosolic face and segregate the ERAD factors EDEM1, OS-9, and SEL1L from the ER lumen. In this Gem, we briefly summarize the current knowledge on ERAD tuning pathways and how they might be hijacked for viral genome replication. As ERAD tuning components, such as SEL1L and nonlipidated LC3, appear to contribute to viral infection, these cellular pathways represent novel candidate drug targets to combat positive-strand RNA viruses.
Indexed as
Identifiers
What OpenQuestion holds
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.