期刊
GENES & DEVELOPMENT
卷 14, 期 22, 页码 2813-2818出版社
COLD SPRING HARBOR LAB PRESS
DOI: 10.1101/gad.813800
关键词
IRF-3; splicing; SR proteins
资金
- NIAID NIH HHS [P01 AI 42257, 5 F32 AI09167-02, P01 AI042257, F32 AI009167] Funding Source: Medline
Interferon regulatory factors constitute a family of transcriptional activators and repressors involved in a large number of vital cellular processes. Interferon regulatory factor-3 (IRF-3) has been implicated in virus and double-stranded RNA mediated induction of IFN beta and RANTES, in DNA damage signaling, and in virus-induced apoptosis. With its critical role in these pathways, the activity of IRF-3 is tightly regulated in myriad ways. Here we describe novel regulation of IRF-3 at the level of RNA splicing. We show that an unprecedented dual utilization of a splice acceptor/donor site within the IRF-3 mRNA governs the production of two alternative splice isoforms.
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