ArticleJournal of virology2013
Foot-and-mouth disease virus 3C protease induces fragmentation of the Golgi compartment and blocks intra-Golgi transport.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Foot-and-mouth disease virus 3C protease as virulence determinant plays multiple roles in cleaving viral polyprotein and host factors.Virulence · 2026Review
- Porcine reproductive and respiratory syndrome virus triggers Golgi apparatus fragmentation-mediated autophagy to facilitate viral self-replication.Journal of virology · 2024Article
- ALS/FTD-associated mutation in cyclin F inhibits ER-Golgi trafficking, inducing ER stress, ERAD and Golgi fragmentation.Scientific reports · 2023Article
- Article
- Foot-and-Mouth Disease Virus: Molecular Interplays with IFN Response and the Importance of the Model.Viruses · 2022Review
- Degradation of Host Proteins and Apoptosis Induced by Foot-and-Mouth Disease Virus 3C Protease.Pathogens (Basel, Switzerland) · 2021Article
- Identification of Potential Drug Targets of Broad-Spectrum Inhibitors with a Michael Acceptor Moiety Using Shotgun Proteomics.Viruses · 2021Review
- Structural Biology of the Enterovirus Replication-Linked 5'-Cloverleaf RNA and Associated Virus Proteins.Microbiology and molecular biology reviews : MMBR · 2020Review
- Biological Function and Application of Picornaviral 2B Protein: A New Target for Antiviral Drug Development.Viruses · 2019Review
- Foot-and-Mouth Disease Virus Antagonizes NOD2-Mediated Antiviral Effects by Inhibiting NOD2 Protein Expression.Journal of virology · 2019Article
- ALS Genetics, Mechanisms, and Therapeutics: Where Are We Now?Frontiers in neuroscience · 2019Review
- Senecavirus A 3C Protease Mediates Host Cell Apoptosis Late in Infection.Frontiers in immunology · 2019Article
- The Different Tactics of Foot-and-Mouth Disease Virus to Evade Innate Immunity.Frontiers in microbiology · 2018Review
- Foot-and-Mouth Disease (FMD) Virus 3C Protease Mutant L127P: Implications for FMD Vaccine Development.Journal of virology · 2017Article
- Knockout of the Golgi stacking proteins GRASP55 and GRASP65 impairs Golgi structure and function.Molecular biology of the cell · 2017Article
- Microtubule Regulation and Function during Virus Infection.Journal of virology · 2017Review
- Hepatitis C virus triggers Golgi fragmentation and autophagy through the immunity-related GTPase M.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- RNA-Dependent RNA Polymerases of Both Virulent and Benign Rabbit Caliciviruses Induce Striking Rearrangement of Golgi Membranes.PloS one · 2017Article
- Influenza infection modulates vesicular trafficking and induces Golgi complex disruption.Virusdisease · 2016Article
- Foot-and-mouth disease virus replicates independently of phosphatidylinositol 4-phosphate and type III phosphatidylinositol 4-kinases.The Journal of general virology · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Picornavirus infection can cause Golgi fragmentation and impose a block in the secretory pathway which reduces expression of major histocompatibility antigens at the plasma membrane and slows secretion of proinflammatory cytokines. In this study, we show that Golgi fragmentation and a block in secretion are induced by expression of foot-and-mouth disease virus (FMDV) 3C(pro) and that this requires the protease activity of 3C(pro). 3C(pro) caused fragmentation of early, medial, and late Golgi compartments, but the most marked effect was on early Golgi compartments, indicated by redistribution of ERGIC53 and membrin. Golgi fragments were dispersed in the cytoplasm and were able to receive a model membrane protein exported from the endoplasmic reticulum (ER). Golgi fragments were, however, unable to transfer the protein to the plasma membrane, indicating a block in intra-Golgi transport. Golgi fragmentation was coincident with a loss of microtubule organization resulting from an inhibition of microtubule regrowth from the centrosome. Inhibition of microtubule regrowth also required 3C(pro) protease activity. The loss of microtubule organization induced by 3C(pro) caused Golgi fragmentation, but loss of microtubule organization does not block intra-Golgi transport. It is likely that the block of intra-Golgi transport is imposed by separate actions of 3C(pro), possibly through degradation of proteins required for intra-Golgi transport.
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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.