ArticleCell reports2021
Lunapark-dependent formation of a virus-induced ER exit site contains multi-tubular ER junctions that promote viral ER-to-cytosol escape.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- SV40 exploits the Nesprin-2-SUN1-KPNA4 axis for stepwise targeting and entry into the host nucleus to promote infection.PLoS pathogens · 2026Article
- Review
- Remodeling of the cellular membrane architecture in response to BK polyomavirus infection.Virology journal · 2026Review
- An ER-associated structure sequesters misassembled FG-rich nucleoporins to help maintain nuclear pore complex function.Journal of cell science · 2025Article
- Reticulophagy and viral infection.Autophagy · 2025Review
- BK Polyomavirus Infection of Bladder Microvascular Endothelial Cells Leads to the Activation of the cGAS-STING Pathway.Journal of medical virology · 2024Article
- The rotavirus VP5*/VP8* conformational transition permeabilizes membranes to Ca2.PLoS pathogens · 2024Article
- Host Subcellular Organelles: Targets of Viral Manipulation.International journal of molecular sciences · 2024Review
- The atlastin ER morphogenic proteins promote formation of a membrane penetration site during non-enveloped virus entry.Journal of virology · 2023Article
- How host ER membrane chaperones and morphogenic proteins support virus infection.Journal of cell science · 2023Article
- Non-enveloped virus membrane penetration: New advances leading to new insights.PLoS pathogens · 2022Article
- Components of the LINC and NPC complexes coordinately target and translocate a virus into the nucleus to promote infection.PLoS pathogens · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Viruses rearrange host membranes to support different entry steps. Polyomavirus simian virus 40 (SV40) reorganizes the endoplasmic reticulum (ER) membrane to generate focus structures that enable virus ER-to-cytosol escape, a decisive infection step. The molecular architecture of the ER exit site that might illuminate why it is ideally suited for membrane penetration is unknown. Here 3D focused ion beam scanning electron microscopy (FIB-SEM) reconstruction reveals that the ER focus structure consists of multi-tubular ER junctions where SV40 preferentially localizes, suggesting that tubular branch points are virus ER-to-cytosol penetration sites. Functional analysis demonstrates that lunapark-an ER membrane protein that typically stabilizes three-way ER junctions-relocates to the ER foci, where it supports focus formation, leading to SV40 ER escape and infection. Our results reveal how a virus repurposes the activity of an ER membrane protein to form a virus-induced ER substructure required for membrane escape and suggest that ER tubular junctions are vulnerable sites exploited by viruses for membrane penetration.
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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.