期刊
NATURE COMMUNICATIONS
卷 4, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms3883
关键词
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资金
- Japan Society for the Promotion of Science
- Ministry of Education, Culture, Sports, Science, and Technology of Japan
- Ministry of Education, Culture, Sports, Science and Technology of Japan [3307]
- Otsuka Pharmaceutical Co., Ltd. - Kyoto University SRP Program
- Banyu Life Science Foundation International
- Takeda Memorial Foundation
- Takeda Memorial Foundation, Suzuken memorial foundation
- Sakakibara memorial foundation
- ONO Medical Research Foundation
- Cell Science Research Foundation
- Daiichi-Sankyo Foundation of Life Science
- Grants-in-Aid for Scientific Research [23390211, 24790753, 24890094, 3307] Funding Source: KAKEN
MicroRNAs (miRs) are small non-protein-coding RNAs that bind to specific mRNAs and inhibit translation or promote mRNA degradation. Recent reports have indicated that miR-33, which is located within the intron of sterol regulatory element-binding protein (SREBP) 2, controls cholesterol homoeostasis and may be a potential therapeutic target for the treatment of atherosclerosis. Here we show that deletion of miR-33 results in marked worsening of high-fat diet-induced obesity and liver steatosis. Using miR-33(-/-) Srebf1(+/-) mice, we demonstrate that SREBP-1 is a target of miR-33 and that the mechanisms leading to obesity and liver steatosis in miR-33(-/-) mice involve enhanced expression of SREBP-1. These results elucidate a novel interaction between SREBP-1 and SREBP-2 mediated by miR-33 in vivo.
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