ArticleJournal of virology2021
The Inflammasome Components NLRP3 and ASC Act in Concert with IRGM To Rearrange the Golgi Apparatus during Hepatitis C Virus Infection.
Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Organelle stress in NLRP3 inflammasome: a central mediator of neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- The role of NLRP3 inflammasome in necrotizing enterocolitis.Pediatric research · 2026Review
- Role of NLRP3 Inflammasomes in Disorders of Children's Digestive Systems: A Narrative Review.Pediatric reports · 2025Review
- Hepatitis C virus-associated cardiomyopathy: A review of pathogenesis.World journal of virology · 2025Article
- Dual role of pyroptosis in liver diseases: mechanisms, implications, and therapeutic perspectives.Frontiers in cell and developmental biology · 2025Review
- H5 subtype avian influenza virus induces Golgi apparatus stress response via TFE3 pathway to promote virus replication.PLoS pathogens · 2024Article
- Functional Role of Hepatitis C Virus NS5A in the Regulation of Autophagy.Pathogens (Basel, Switzerland) · 2024Review
- Article
- Structural basis for the oligomerization-facilitated NLRP3 activation.Nature communications · 2024Article
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- The role of inflammasome in chronic viral hepatitis.Frontiers in cellular and infection microbiology · 2024Review
- HCV-induced autophagy and innate immunity.Frontiers in immunology · 2024Review
- Polydatin-Mediated Inhibition of HSP90α Disrupts NLRP3 Complexes and Alleviates Acute Pancreatitis.Research (Washington, D.C.) · 2024Article
- Drugging the NLRP3 inflammasome: from signalling mechanisms to therapeutic targets.Nature reviews. Drug discovery · 2024Review
- Review
- Comprehensive protocols for culturing and molecular biological analysis of IBD patient-derived colon epithelial organoids.Frontiers in immunology · 2023Article
- Uncoupled pyroptosis and IL-1β secretion downstream of inflammasome signaling.Frontiers in immunology · 2023Review
- Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis.Viruses · 2022Review
- Review
- Structure modeling hints at a granular organization of the Golgi ribbon.BMC biology · 2022Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) infection triggers Golgi fragmentation through the Golgi-resident protein immunity-related GTPase M (IRGM). Here, we report the roles of NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) and ASC (apoptosis-associated speck-like protein containing a caspase activation and recruitment domain [CARD]), two inflammasome components, in the initial events leading to this fragmentation. We show that ASC resides at the Golgi with IRGM at homeostasis. Upon infection, ASC dissociates from both IRGM and the Golgi and associates with HCV-induced NLRP3. NLRP3 silencing inhibits Golgi fragmentation. ASC silencing disrupts the Golgi structure in both control and infected cells and reduces the localization of IRGM at the Golgi. IRGM depletion in the ASC-silenced cells cannot totally restore the Golgi structure. These data highlight a role for ASC, upstream of the formation of the inflammasome, in regulating IRGM through its control on the Golgi. A similar mechanism occurs in response to nigericin treatment, but not in cells infected with another member of the
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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.