2. Academic Validation
  3. Negative regulation of virus-triggered IFN-beta signaling pathway by alternative splicing of TBK1

Negative regulation of virus-triggered IFN-beta signaling pathway by alternative splicing of TBK1

  • J Biol Chem. 2008 Dec 19;283(51):35590-7. doi: 10.1074/jbc.M805775200.
Weiwen Deng 1,  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
Affiliations

Affiliation

  • 1 Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
PMID: 18977754 DOI: 10.1074/jbc.M805775200
Abstract

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-beta production. Taken together, our data indicate that TBK1s plays an inhibitory role in virus-triggered IFN-beta signaling pathways.

Figures