The favorable IFNL3 genotype escapes mRNA decay mediated by AU-rich elements and hepatitis C virus-induced microRNAs.

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Published in Nat Immunol on November 17, 2013

Authors

Adelle P McFarland1, Stacy M Horner2, Abigail Jarret1, Rochelle C Joslyn1, Eckart Bindewald3, Bruce A Shapiro4, Don A Delker5, Curt H Hagedorn6, Mary Carrington7, Michael Gale1, Ram Savan1

Author Affiliations

1: Department of Immunology, University of Washington, Seattle, Washington, USA.
2: 1] Department of Immunology, University of Washington, Seattle, Washington, USA. [2].
3: Basic Science Program, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA.
4: Center for Cancer Research Nanobiology Program, National Cancer Institute, Frederick, Maryland, USA.
5: Divison of Gastroenterology, Hepatology and Nutrition, School of Medicine, University of Utah, Salt Lake City, Utah, USA.
6: 1] Divison of Gastroenterology, Hepatology and Nutrition, School of Medicine, University of Utah, Salt Lake City, Utah, USA. [2].
7: 1] Cancer and Inflammation Program, Laboratory of Experimental Immunology, Science Applications International Corporation-Frederick, Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA. [2] Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Boston, Massachusetts, USA.

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