ArticleCellular microbiology2010
Poliovirus replication requires the N-terminus but not the catalytic Sec7 domain of ArfGEF GBF1.
Article in Cellular microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 64 citations in OpenAlex.
- Infection-specific long-chain fatty acid metabolism as a broad anti-enterovirus target.bioRxiv : the preprint server for biology · 2026Article
- Broad-spectrum antiviral activity of antisense oligonucleotides targeting GBF1 against SARS-CoV-2 and influenza viruses.iScience · 2026Article
- 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
- The Arf-GEF GBF1 undergoes multi-domain structural shifts to activate Arf at the Golgi.Frontiers in cell and developmental biology · 2023Article
- A Proximity biotinylation assay with a host protein bait reveals multiple factors modulating enterovirus replication.PLoS pathogens · 2022Article
- 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
- De Novo and Inherited Variants in GBF1 are Associated with Axonal Neuropathy Caused by Golgi Fragmentation.American journal of human genetics · 2020Article
- SON DNA-binding protein mediates macrophage autophagy and responses to intracellular infection.FEBS letters · 2020Article
- Role of the Guanine Nucleotide Exchange Factor GBF1 in the Replication of RNA Viruses.Viruses · 2020Review
- Quantitative Proteomics of Uukuniemi Virus-host Cell Interactions Reveals GBF1 as Proviral Host Factor for Phleboviruses.Molecular & cellular proteomics : MCP · 2019Article
- A Redundant Mechanism of Recruitment Underlies the Remarkable Plasticity of the Requirement of Poliovirus Replication for the Cellular ArfGEF GBF1.Journal of virology · 2019Article
- The Guanine Nucleotide Exchange Factor GBF1 Participates in Rotavirus Replication.Journal of virology · 2019Article
- Functional and Physical Interaction between the Arf Activator GBF1 and Hepatitis C Virus NS3 Protein.Journal of virology · 2019Article
- Newcastle Disease Virus-Based Vectored Vaccine against Poliomyelitis.Journal of virology · 2018Article
- Highly conserved motifs within the large Sec7 ARF guanine nucleotide exchange factor GBF1 target it to the Golgi and are critical for GBF1 activity.American journal of physiology. Cell physiology · 2018Article
- N-Terminomics TAILS Identifies Host Cell Substrates of Poliovirus and Coxsackievirus B3 3C Proteinases That Modulate Virus Infection.Journal of virology · 2018Article
- Identification of GBF1 as a cellular factor required for hepatitis E virus RNA replication.Cellular microbiology · 2018Article
- Enterovirus 3A Facilitates Viral Replication by Promoting Phosphatidylinositol 4-Kinase IIIβ-ACBD3 Interaction.Journal of virology · 2017Article
- The Golgi protein ACBD3 facilitates Enterovirus 71 replication by interacting with 3A.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Viruses are intracellular parasites whose reproduction relies on factors provided by the host. The cellular protein GBF1 is critical for poliovirus replication. Here we show that the contribution of GBF1 to virus replication is different from its known activities in uninfected cells. Normally GBF1 activates the ADP-ribosylation factor (Arf) GTPases necessary for formation of COPI transport vesicles. GBF1 function is modulated by p115 and Rab1b. However, in polio-infected cells, p115 is degraded and neither p115 nor Rab1b knock-down affects virus replication. Poliovirus infection is very sensitive to brefeldin A (BFA), an inhibitor of Arf activation by GBF1. BFA targets the catalytic Sec7 domain of GBF1. Nevertheless the BFA block of polio replication is rescued by expression of only the N-terminal region of GBF1 lacking the Sec7 domain. Replication of BFA-resistant poliovirus in the presence of BFA is uncoupled from Arf activation but is dependent on GBF1. Thus the function(s) of this protein essential for viral replication can be separated from those required for cellular metabolism.
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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.