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mmu-mir-122: A study using mouse models for non-alcoholic fatty liver disease (NAFLD) found that liver cells exposed to excessive lipids released higher numbers of exosomes containing higher amounts of mmu-mir-122 and mmu-miR-192 [PMC7936154]. The motif corresponding to the seed of mmu-mir-122 was significantly overrepresented in the 3′UTRs of upregulated genes and underrepresented in the 3′UTRs of downregulated genes [PMC2820085]. Inhibition of mmu-mir-122 was found to be the primary cause for up-regulation of 372 genes, with 11% of these genes predicted to contain a perfect 8-mer binding site for mmu-mir-122 [PMC3125776]. In mice infected with S. japonicum, serum levels of mmu-miR-21, mmu-mir-122, and mmumiR-34a were significantly higher [PMC9650547]. Treatment with PB decreased hepatic levels of mmu-mir-122 in mice [PMC3399820]. Kupffer cells were found to express specific miRNAs including mmu-mir-122 [PMC8652219]. The expression levels of miR-122 were measured using real-time RT-qPCR and TaqMan assays [PMC3399820][PMC8652219][PMC8935237][PMC4569899]. Transfection with an anti-sense oligonucleotide inhibitor increased mRNA expression levels for six genes including GYS1, SLC7A1, MINK1, ALDOA, CCNG1, and P4HA1 in a mouse hepatocyte-derived cell line [PMC5415838]. Down-regulation of mmu-mir-122 during high-fat diet (HFD)-induced obesity was observed in mice [PMC3319598]. Mmu-mir-122 is mainly expressed in the liver and constitutes 70% of all liver miRNAs [PMC3319598].
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