Negative Regulation of Virus-triggered IFN-β Signaling Pathway by Alternative Splicing of TBK1

Induction of Type I IFNs is a central event in antiviral responses and must be tightly controlled. The protein kinase TBK1 is critically involved in virus-triggered type I IFN signaling. In this study, we identify an alternatively spliced isoform of TBK1, termed TBK1s, which lacks exons 3–6. Upon...

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Published inThe Journal of biological chemistry Vol. 283; no. 51; p. 35590
Main Authors Weiwen Deng, Mude Shi, Meifang Han, Jin Zhong, Zhenhu Li, Weina Li, Yu Hu, Lingchen Yan, Jie Wang, Ying He, Hong Tang, Vincent Deubel, Xiaoping Luo, Qin Ning, Bing Sun
Format Journal Article
LanguageEnglish
Published American Society for Biochemistry and Molecular Biology 19.12.2008
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Summary:Induction of Type I IFNs is a central event in antiviral responses and must be tightly controlled. The protein kinase TBK1 is critically involved in virus-triggered type I IFN signaling. In this study, we identify an alternatively spliced isoform of TBK1, termed TBK1s, which lacks exons 3–6. Upon Sendai virus (SeV) infection, TBK1s is induced in both human and mouse cells and binds to RIG-1, disrupting the interaction between RIG-I and VISA. Consistent with that result, overexpression of TBK1s inhibits IRF3 nuclear translocation and leads to a shutdown of SeV-triggered IFN-β production. Taken together, our data indicate that TBK1s plays an inhibitory role in virus-triggered IFN-β signaling pathways.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.M805775200