Journal
NATURE IMMUNOLOGY
Volume 13, Issue 6, Pages 543-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2291
Keywords
-
Categories
Funding
- Canadian Institutes of Health Research [MOP-7214]
- US National Institutes of Health [AI 073898, GM056927, T32 AI007647]
- Irma Hirschl Trust
Ask authors/readers for more resources
Type I interferon is an integral component of the antiviral response, and its production is tightly controlled at the levels of transcription and translation. The eukaryotic translation-initiation factor eIF4E is a rate-limiting factor whose activity is regulated by phosphorylation of Ser209. Here we found that mice and fibroblasts in which eIF4E cannot be phosphorylated were less susceptible to virus infection. More production of type I interferon, resulting from less translation of Nfkbia mRNA (which encodes the inhibitor I kappa B alpha), largely explained this phenotype. The lower abundance of IkBa resulted in enhanced activity of the transcription factor NF-kappa B, which promoted the production of interferon-beta (IFN-beta). Thus, regulated phosphorylation of eIF4E has a key role in antiviral host defense by selectively controlling the translation of an mRNA that encodes a critical suppressor of the innate antiviral response.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available