id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-326217-ji0njeha	Saleh, Maged	Glycogen Synthase Kinase 3β Enhances Hepatitis C Virus Replication by Supporting miR-122	2018-11-27		.txt	text/plain	4731	262	48	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. To assess whether both GSK3 isoforms are required for HCV replication, we silenced GSK3α and / or GSK3β gene expression by transfecting siRNAs and quantified HCV RNA in Huh-7.5 cells harboring HCV subgenomic replicon (Con1) or infectious HCV (Jc1). Given the well-known dependency of HCV on miR-122 (Jopling et al., 2005 (Jopling et al., , 2008 Machlin et al., 2011) and the regulatory circuit between insulin-like growth factor 1 receptor, GSK3β, and miR-122 identified previously (Zeng et al., 2010) , we assessed the effect of GSK3 inhibition on miR-122 expression in Huh-7.5 cells harboring a subgenomic HCV replicon.	./cache/cord-326217-ji0njeha.txt	./txt/cord-326217-ji0njeha.txt