期刊
GENES & DEVELOPMENT
卷 29, 期 15, 页码 1599-1604出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.263749.115
关键词
Argonaute; RISC; hnRNP D; microRNA; ribonucleoprotein complex
资金
- National Institute on Aging-Intramural Research Program (National Institutes of Health)
- American Heart Association grant [11PRE6900008]
- National Institutes of Health grant [R01 CA102428]
- National Institute of Arthritis and Musculoskeletal and Skin Diseases-Intramural Research Program (National Institutes of Health)
- Charles H. Revson Foundation
- Howard Hughes Medical Institute
- Starr Cancer Foundation
- Creative Research Initiatives (Physical Genetics Laboratory) of the National Research Foundation of Korea [2009-0081562]
- Korean Ministry of Science, ICT, and Future Planning [NRF-M1AXA002-2011-0031416, 2011-0031955, N1014002]
- NATIONAL CANCER INSTITUTE [R01CA102428] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [ZIAAR041200] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [ZICAG000616, ZIAAG000393] Funding Source: NIH RePORTER
Eukaryotic gene expression is tightly regulated post-transcriptionally by RNA-binding proteins (RBPs) and microRNAs. The RBP AU-rich-binding factor 1 (AUF1) isoform p37 was found to have high affinity for the microRNA let-7b in vitro (K-d = similar to 6 nM) in cells. Ribonucleoprotein immunoprecipitation, in vitro association, and single-molecule-binding analyses revealed that AUF1 promoted let-7b loading onto Argonaute 2 (AGO2), the catalytic component of the RNA-induced silencing complex (RISC). In turn, AGO2-let-7 triggered target mRNA decay. Our findings uncover a novel mechanism by which AUF1 binding and transfer of microRNA let-7 to AGO2 facilitates let-7-elicited gene silencing.
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