ArticleThe Journal of biological chemistry2014
The hepatitis C virus core protein inhibits adipose triglyceride lipase (ATGL)-mediated lipid mobilization and enhances the ATGL interaction with comparative gene identification 58 (CGI-58) and lipid droplets.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Chronic viral hepatitis with concurrent metabolic dysfunction-associated steatotic liver disease: dual etiology challenges.Clinical and molecular hepatology · 2026Review
- Induction of phospholipase A2 group 4C by HCV infection regulates lipid droplet formation.JHEP reports : innovation in hepatology · 2025Article
- White spot syndrome virus (WSSV) modulates lipid metabolism in white shrimp.Communications biology · 2023Article
- Lipid Droplet-Associated Proteins Perilipin 1 and 2: Molecular Markers of Steatosis and Microvesicular Steatotic Foci in Chronic Hepatitis C.International journal of molecular sciences · 2022Article
- Lipolysis: cellular mechanisms for lipid mobilization from fat stores.Nature metabolism · 2021Review
- Very-long-chain fatty acid metabolic capacity of 17-beta-hydroxysteroid dehydrogenase type 12 (HSD17B12) promotes replication of hepatitis C virus and related flaviviruses.Scientific reports · 2020Article
- CGI-58: Versatile Regulator of Intracellular Lipid Droplet Homeostasis.Advances in experimental medicine and biology · 2020Review
- Foam Cells: One Size Doesn't Fit All.Trends in immunology · 2019Review
- Methods for Lipid Droplet Biophysical Characterization inFrontiers in microbiology · 2018Review
- Critical roles for α/β hydrolase domain 5 (ABHD5)/comparative gene identification-58 (CGI-58) at the lipid droplet interface and beyond.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017Review
- Lipid droplets and liver disease: from basic biology to clinical implications.Nature reviews. Gastroenterology & hepatology · 2017Review
- The lipid droplet-associated protein perilipin 3 facilitates hepatitis C virus-driven hepatic steatosis.Journal of lipid research · 2017Article
- Modulation of Lipid Droplet Metabolism-A Potential Target for Therapeutic Intervention inFrontiers in microbiology · 2017Review
- Structure, Function and Metabolism of Hepatic and Adipose Tissue Lipid Droplets: Implications in Alcoholic Liver Disease.Current molecular pharmacology · 2017Review
- Properties and Functions of the Dengue Virus Capsid Protein.Annual review of virology · 2016Review
- Entangled in a membranous web: ER and lipid droplet reorganization during hepatitis C virus infection.Current opinion in cell biology · 2016Review
- Hepatitis C Virus-Induced Degradation of Cell Death-Inducing DFFA-Like Effector B Leads to Hepatic Lipid Dysregulation.Journal of virology · 2016Article
- Article
- Hepatitis C Virus Increases Occludin Expression via the Upregulation of Adipose Differentiation-Related Protein.PloS one · 2016Article
- Hepatic lipid droplet biology: Getting to the root of fatty liver.Hepatology (Baltimore, Md.) · 2015Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Liver steatosis is a common health problem associated with hepatitis C virus (HCV) and an important risk factor for the development of liver fibrosis and cancer. Steatosis is caused by triglycerides (TG) accumulating in lipid droplets (LDs), cellular organelles composed of neutral lipids surrounded by a monolayer of phospholipids. The HCV nucleocapsid core localizes to the surface of LDs and induces steatosis in cultured cells and mouse livers by decreasing intracellular TG degradation (lipolysis). Here we report that core at the surface of LDs interferes with the activity of adipose triglyceride lipase (ATGL), the key lipolytic enzyme in the first step of TG breakdown. Expressing core in livers or mouse embryonic fibroblasts of ATGL(-/-) mice no longer decreases TG degradation as observed in LDs from wild-type mice, supporting the model that core reduces lipolysis by engaging ATGL. Core must localize at LDs to inhibit lipolysis, as ex vivo TG hydrolysis is impaired in purified LDs coated with core but not when free core is added to LDs. Coimmunoprecipitation experiments revealed that core does not directly interact with the ATGL complex but, unexpectedly, increased the interaction between ATGL and its activator CGI-58 as well as the recruitment of both proteins to LDs. These data link the anti-lipolytic activity of the HCV core protein with altered ATGL binding to CGI-58 and the enhanced association of both proteins with LDs.
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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.