ArticlePLoS pathogens2008
A critical role of a cellular membrane traffic protein in poliovirus RNA replication.
Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 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.
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Who cites it
105 citing papers in PubMed, 130 citations in OpenAlex.
- Poliovirus 3Dpol polymerase region is essential for cleavage of poliovirus 3AB in vivo.PLoS pathogens · 2026Article
- Genotype-by-inhibitor interactions to dissect enterovirus replication.Nature communications · 2026Article
- Mechanical Cues Regulate Cargo Sorting and Export at the Golgi.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Genotype-by-Inhibitor Interactions to Dissect Enterovirus Replication.Research square · 2025Article
- An efficientJournal of virology · 2024Article
- The development of resistance to an inhibitor of a cellular protein reveals a critical interaction between the enterovirus protein 2C and a small GTPase Arf1.PLoS pathogens · 2023Article
- Site-specific phosphorylations of the Arf activator GBF1 differentially regulate GBF1 function in Golgi homeostasis and secretion versus cytokinesis.Scientific reports · 2023Article
- The Arf-GEF GBF1 undergoes multi-domain structural shifts to activate Arf at the Golgi.Frontiers in cell and developmental biology · 2023Article
- Viral protein engagement of GBF1 induces host cell vulnerability through synthetic lethality.The Journal of cell biology · 2022Article
- Control of infection by LC3-associated phagocytosis, CASM, and detection of raised vacuolar pH by the V-ATPase-ATG16L1 axis.Science advances · 2022Review
- A Proximity biotinylation assay with a host protein bait reveals multiple factors modulating enterovirus replication.PLoS pathogens · 2022Article
- AG1478 Elicits a Novel Anti-Influenza Function via an EGFR-Independent, GBF1-Dependent Pathway.International journal of molecular sciences · 2022Article
- Rab1b-GBF1-ARF1 Secretory Pathway Axis Is Required for Birnavirus Replication.Journal of virology · 2022Article
- Review
- Secretory Carrier Membrane Protein 3 Interacts with 3A Viral Protein of Enterovirus and Participates in Viral Replication.Microbiology spectrum · 2021Article
- A comparative analysis of parechovirus protein structures with other picornaviruses.Open biology · 2021Article
- Picornaviruses: A View from 3A.Viruses · 2021Review
- Enterovirus Infection Induces Massive Recruitment of All Isoforms of Small Cellular Arf GTPases to the Replication Organelles.Journal of virology · 2020Article
- Double-Membrane Vesicles as Platforms for Viral Replication.Trends in microbiology · 2020Review
- Viral protein engagement of GBF1 induces host cell vulnerability through synthetic lethality.bioRxiv : the preprint server for biology · 2020Article
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Replication of many RNA viruses is accompanied by extensive remodeling of intracellular membranes. In poliovirus-infected cells, ER and Golgi stacks disappear, while new clusters of vesicle-like structures form sites for viral RNA synthesis. Virus replication is inhibited by brefeldin A (BFA), implicating some components(s) of the cellular secretory pathway in virus growth. Formation of characteristic vesicles induced by expression of viral proteins was not inhibited by BFA, but they were functionally deficient. GBF1, a guanine nucleotide exchange factor for the small cellular GTPases, Arf, is responsible for the sensitivity of virus infection to BFA, and is required for virus replication. Knockdown of GBF1 expression inhibited virus replication, which was rescued by catalytically active protein with an intact N-terminal sequence. We identified a mutation in GBF1 that allows growth of poliovirus in the presence of BFA. Interaction between GBF1 and viral protein 3A determined the outcome of infection in the presence of BFA.
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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.