>Csf3r|NM_007782|3'UTR
   1 AACTTTGGGGGTCCTTGTATCTTGAAGACCCTGCCCTATTCAGAGGAGAAGAGCCCTCCGCTGAAATCTACTGGCCCTGA
  81 GAGAAGCAGAAAGGCCCAGTGTGTCTCTGTCTCTGGCCCCTAGCACCTCTCCTCTACTCTGAGCTTCTCAGGCTATACCC
 161 TGAGGTCACCCACTCTCACACTCTAAGGTTCAGATAGATACTGCTTACAGCCCAATGGTCACCATTCGTCTTTCATATAA
 241 TTTCAGTCCATTGAACTGATTGTAGGTTTTGAGTTGGGGCTGGTATTTTCAGAAATTCTGGCTGGACGTGGTGGTACATG
 321 CCTAGCATCCCAACATCTGGGAGGAAGATGCAGGAAGATTGCAAGTTCCAGGCCAGCCTGGGCTAGCCTACATAGTGAGA
 401 TCCAATCTCAAAAATTATGCTGGGTGTGGTGGTGCATGCCTTTAATCCCAGCACTCGGGAGGCAGAGGCAGGTAGATTTC
 481 TGAGTTCGAGGCCAGCCTGGTCTACAAAGTGAGTTCCAGGACAGCCAGGGCTATACAGAGAAACCCTGTCTTGAAAAAAA
 561 AAATTAAGCAAAAGCTGAATAAATAAAGTTTTTTTTATGACATGTACTTGTTTTGTGGGGAGTGGGGATTCAGAGGCAGA
 641 GGTCAGAAGACACCTACCTTGTGGGAATTAACTCTGGTCTCCAGCATGTGGATCTTGAGAAGTGGACTCAAAGCTTAGTG
 721 ACAAGCACCGCGTTACCCATGGAGGCATCTTATTGGTCCCAGAAAAGAATCTCTTGAGCATAGCTTAAGTGTCTTCTACC
 801 CTTGTTTGTTTTTTGTCTCTGCTTGCTTGTTTTTCTTTTTATGTATTATAAATAAGTACAATGTTGCTGTCTTCAGACAC
 881 ACCAGAAGAGGGCATCAGATCTCAATACTGGTGGTTGTGAACCACCATGTGGTTGCTGGGATTTGAATTTAGGACCTTTG
 961 GAAGAGCAGTCAGTGCTCCTACCCGCTGAGCCATCTCTTCAGTCCAGTTTATTTGTTTTTCAAGACAGGGTTTCTCTGTG
1041 TAACAGCCCAACCTATCCTGGAACTTACTCTATAGATCAGGCTGGCCTCAAGATCCACCTGCCTCTGCCTTAAATGCTGG
1121 GAATAAAGGTGTGCACC

ID	Duplex structure	Position	Score	MFE
1	miRNA 3' guuuGU-GGUAACAGUGUGAGGu 5' || ||| | ||||||||: Target 5' aggtCACCCACTCTCACACTCTa 3'	163 - 185	150.00	-18.10
2	miRNA 3' guUUGUGGUAACAG-----UGUGAGGu 5' ||::::: |||| |||| || Target 5' acAATGTTGCTGTCTTCAGACACACCa 3'	858 - 884	124.00	-12.90
3	miRNA 3' guuUGUGGUAA-CAG---UGUGAGgu 5' |::|| || || :||||| Target 5' tgcATGCCTTTAATCCCAGCACTCgg 3'	433 - 458	115.00	-7.20

- The Journal of clinical investigation, 2012

MicroRNA-122 (miR-122), which accounts for 70% of the liver's total miRNAs, plays a pivotal role in the liver. However, its intrinsic physiological roles remain largely undetermined. We demonstrated that mice lacking the gene encoding miR-122a (Mir122a) are viable but develop temporally controlled steatohepatitis, fibrosis, and hepatocellular carcinoma (HCC). These mice exhibited a striking disparity in HCC incidence based on sex, with a male-to-female ratio of 3.9:1, which recapitulates the disease incidence in humans. Impaired expression of microsomal triglyceride transfer protein (MTTP) contributed to steatosis, which was reversed by in vivo restoration of Mttp expression. We found that hepatic fibrosis onset can be partially attributed to the action of a miR-122a target, the Klf6 transcript. In addition, Mir122a(-/-) livers exhibited disruptions in a range of pathways, many of which closely resemble the disruptions found in human HCC. Importantly, the reexpression of miR-122a reduced disease manifestation and tumor incidence in Mir122a(-/-) mice. This study demonstrates that mice with a targeted deletion of the Mir122a gene possess several key phenotypes of human liver diseases, which provides a rationale for the development of a unique therapy for the treatment of chronic liver disease and HCC.