{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xu H"],"funding":["National Basic Research Program of China","National Key R&D Program of China","National Natural Science Foundation of China","Natural Science Foundation of Guangdong Province"],"pagination":["e41159"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6389286"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8"],"pubmed_abstract":["MicroRNA-122 (miR-122) is the most abundant microRNA in hepatocytes and a central player in liver biology and disease. Herein, we report a previously unknown role for miR-122 in hepatocyte intrinsic innate immunity. Restoration of miR-122 levels in hepatoma cells markedly enhanced the activation of interferons (IFNs) in response to a variety of viral nucleic acids or simulations, especially in response to hepatitis C virus RNA and poly (I:C). Mechanistically, miR-122 downregulated the phosphorylation (Tyr705) of STAT3, thereby removing the negative regulation of STAT3 on IFN-signaling. STAT3 represses IFN expression by inhibiting interferon regulatory factor 1 (IRF1), whereas miR-122 targets MERTK, FGFR1 and IGF1R, three receptor tyrosine kinases (RTKs) that directly promote STAT3 phosphor"],"journal":["eLife"],"pubmed_title":["MicroRNA-122 supports robust innate immunity in hepatocytes by targeting the RTKs/STAT3 signaling pathway."],"pmcid":["PMC6389286"],"funding_grant_id":["31200593","2017YFA0504400","31471223","2011CB811300","31671349","31230042","2014A030313163"],"pubmed_authors":["Xie SJ","Yang JH","Qu LH","Zhang Y","Xu SJ","Zheng MN","Zhang WQ","Xu H","Zhou H"],"additional_accession":[]},"is_claimable":false,"name":"MicroRNA-122 supports robust innate immunity in hepatocytes by targeting the RTKs/STAT3 signaling pathway.","description":"MicroRNA-122 (miR-122) is the most abundant microRNA in hepatocytes and a central player in liver biology and disease. Herein, we report a previously unknown role for miR-122 in hepatocyte intrinsic innate immunity. Restoration of miR-122 levels in hepatoma cells markedly enhanced the activation of interferons (IFNs) in response to a variety of viral nucleic acids or simulations, especially in response to hepatitis C virus RNA and poly (I:C). Mechanistically, miR-122 downregulated the phosphorylation (Tyr705) of STAT3, thereby removing the negative regulation of STAT3 on IFN-signaling. STAT3 represses IFN expression by inhibiting interferon regulatory factor 1 (IRF1), whereas miR-122 targets MERTK, FGFR1 and IGF1R, three receptor tyrosine kinases (RTKs) that directly promote STAT3 phosphor","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Feb","modification":"2026-05-04T08:03:04.521Z","creation":"2019-06-06T23:24:08Z"},"accession":"S-EPMC6389286","cross_references":{"pubmed":["30735121"],"doi":["10.7554/eLife.41159"]}}