About: Glycogen Synthase Kinase 3β Enhances Hepatitis C Virus Replication by Supporting miR-122

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About: Glycogen Synthase Kinase 3β Enhances Hepatitis C Virus Replication by Supporting miR-122 Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Glycogen Synthase Kinase 3β Enhances Hepatitis C Virus Replication by Supporting miR-122
Creator	Chan, Shiu-Wan Li, Yize Gouttenoire, Jérôme Moradpour, Darius Rüschenbaum, Sabrina Saleh, Maged Welsch, Christoph Zeuzem, Stefan Lange, Christian Sato, Yoshitaka
Source	Medline; PMC
abstract	Hepatitis C virus (HCV) infection is associated with alterations in host lipid and insulin signaling cascades, which are partially explained by a dependence of the HCV life cycle on key molecules in these metabolic pathways. Yet, little is known on the role in the HCV life cycle of glycogen synthase kinase 3 (GSK3), one of the most important kinases in cellular metabolism. Therefore, the impact of GSK3 on the HCV life cycle was assessed in human hepatoma cell lines harboring subgenomic genotype 1b and 2a replicons or producing cell culture-derived HCV genotype 2a by exposure to synthetic GSK3 inhibitors, GSK3 gene silencing, overexpression of GSK3 constructs and immunofluorescence analyses. In addition, the role of GSK3 in hepatitis E virus (HEV) replication was investigated to assess virus specificity of the observed findings. We found that both inhibition of GSK3 function by synthetic inhibitors as well as silencing of GSK3β gene expression resulted in a decrease of HCV replication and infectious particle production, whereas silencing of the GSK3α isoform had no relevant effect on the HCV life cycle. Conversely, overexpression of GSK3β resulted in enhanced HCV replication. In contrast, GSK3β had no effect on replication of subgenomic HEV replicon. The pro-viral effect of GSK3β on HCV replication was mediated by supporting expression of microRNA-122 (miR-122), a micro-RNA which is mandatory for wild-type HCV replication, as GSK3 inhibitors suppressed miR-122 levels and as inhibitors of GSK3 had no antiviral effect on a miR-122-independent HCV mutant. In conclusion, we have identified GSK3β is a novel host factor supporting HCV replication by maintaining high levels of hepatic miR-122 expression.
has issue date	2018-11-27(xsd:dateTime)
bibo:doi	10.3389/fmicb.2018.02949
bibo:pmid	30542341
has license	cc-by
sha1sum (hex)	80beb71c4b247cf32525097f28568b49f71cf08b
schema:url	https://doi.org/10.3389/fmicb.2018.02949
resource representing a document's title	Glycogen Synthase Kinase 3β Enhances Hepatitis C Virus Replication by Supporting miR-122
has PubMed Central identifier	PMC6278592
has PubMed identifier	30542341
schema:publication	Front Microbiol
resource representing a document's body	covid:80beb71c4b247cf32525097f28568b49f71cf08b#body_text
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