ArticleJournal of virology2007
Activation of cellular Arf GTPases by poliovirus protein 3CD correlates with virus replication.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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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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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
47 citing papers in PubMed, 67 citations in OpenAlex.
- The MNV-1 protease-polymerase precursor cleaves a novel site in the NS1-2 protein.The Journal of general virology · 2026Article
- Article
- Non-lytic spread of poliovirus requires the nonstructural protein 3CD.bioRxiv : the preprint server for biology · 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
- Defining the proximal interaction networks of Arf GTPases reveals a mechanism for the regulation of PLD1 and PI4KB.The EMBO journal · 2022Article
- Role of Host Small GTPases in Apicomplexan Parasite Infection.Microorganisms · 2022Review
- Enterovirus 71 Activates GADD34 via Precursor 3CD to Promote IRES-Mediated Viral Translation.Microbiology spectrum · 2022Article
- Picornaviruses: A View from 3A.Viruses · 2021Review
- Article
- Development of a Viral RdRp-Assisted Gene Silencing System and Its Application in the Identification of Host Factors of Plant (+)RNA Virus.Frontiers in microbiology · 2021Article
- Zika NS1-induced ER remodeling is essential for viral replication.The Journal of cell biology · 2020Article
- Enterovirus Replication Organelles and Inhibitors of Their Formation.Frontiers in microbiology · 2020Review
- Newcastle Disease Virus-Based Vectored Vaccine against Poliomyelitis.Journal of virology · 2018Article
- Host lipidome analysis during rhinovirus replication in HBECs identifies potential therapeutic targets.Journal of lipid research · 2018Article
- Hijacking of multiple phospholipid biosynthetic pathways and induction of membrane biogenesis by a picornaviral 3CD protein.PLoS pathogens · 2018Article
- Multiple poliovirus-induced organelles suggested by comparison of spatiotemporal dynamics of membranous structures and phosphoinositides.PLoS pathogens · 2018Article
- The RNA-Binding Site of Poliovirus 3C Protein Doubles as a Phosphoinositide-Binding Domain.Structure (London, England : 1993) · 2017Article
- Investigation of the Role of Protein Kinase D in Human Rhinovirus Replication.Journal of virology · 2017Article
- Endoplasmic Reticulum: The Favorite Intracellular Niche for Viral Replication and Assembly.Viruses · 2016Review
- Mechanisms of Beta Cell Dysfunction Associated With Viral Infection.Current diabetes reports · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
We have previously shown that synthesis of poliovirus protein 3CD in uninfected HeLa cell extracts induces an increased association with membranes of the cellular Arf GTPases, which are key players in cellular membrane traffic. Arfs cycle between an inactive, cytoplasmic, GDP-bound form and an active, membrane-associated, GTP-bound form. 3CD promotes binding of Arf to membranes by initiating recruitment to membranes of guanine nucleotide exchange factors (GEFs), BIG1 and BIG2. GEFs activate Arf by replacing GDP with GTP. In poliovirus-infected cells, there is a dramatic redistribution of cellular Arf pools that coincides with the reorganization of membranes used to form viral RNA replication complexes. Here we demonstrate that Arf translocation in vitro can be induced by purified recombinant 3CD protein; thus, concurrent translation of viral RNA is not required. Coexpression of 3C and 3D proteins was not sufficient to target Arf to membranes. 3CD expressed in HeLa cells was retained after treatment of the cells with digitonin, indicating that it may interact with a membrane-bound host factor. A F441S mutant of 3CD was shown previously to have lost Arf translocation activity and was also defective in attracting the corresponding GEFs to membranes. A series of other mutations were introduced at 3CD residue F441. Mutations that retained Arf translocation activity of 3CD also supported efficient growth of virus, regardless of their effects on 3D polymerase elongation activity. Those that abrogated Arf activation by 3CD generated quasi-infectious RNAs that produced some plaques from which revertants that always restored the Arf activation property of 3CD were rescued.
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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.