期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 283, 期 51, 页码 35590-35597出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M805775200
关键词
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资金
- National Natural Science Foundation of China [30325018, 30530700, 30623003, 30421005]
- CAS Project [KSCX1-YW-R-43]
- National Key Project 973 [2005CB522901, 2006CB504300, 2007CB512404, 2007CB512900]
- Technology Commission of Shanghai Municipality [04DZ14902, 04DZ19108, 06DZ22032, 04DZ19112, 07XD14033, 064319034, 07DZ22916]
- 863 key projects [2006AA02A247]
- Ministry of Health of China [2008ZX10206]
- EU [SP5B-CT-2006-044161]
- E-institutes of Shanghai Universities, Immunology Division
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.
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