|  Help  |  About  |  Contact Us

Publication : Critical role of TRAF3 in the Toll-like receptor-dependent and -independent antiviral response.

First Author  Oganesyan G Year  2006
Journal  Nature Volume  439
Issue  7073 Pages  208-11
PubMed ID  16306936 Mgi Jnum  J:245346
Mgi Id  MGI:5918298 Doi  10.1038/nature04374
Citation  Oganesyan G, et al. (2006) Critical role of TRAF3 in the Toll-like receptor-dependent and -independent antiviral response. Nature 439(7073):208-11
abstractText  Type I interferon (IFN) production is a critical component of the innate defence against viral infections. Viral products induce strong type I IFN responses through the activation of Toll-like receptors (TLRs) and intracellular cytoplasmic receptors such as protein kinase R (PKR). Here we demonstrate that cells lacking TRAF3, a member of the TNF receptor-associated factor family, are defective in type I IFN responses activated by several different TLRs. Furthermore, we show that TRAF3 associates with the TLR adaptors TRIF and IRAK1, as well as downstream IRF3/7 kinases TBK1 and IKK-epsilon, suggesting that TRAF3 serves as a critical link between TLR adaptors and downstream regulatory kinases important for IRF activation. In addition to TLR stimulation, we also show that TRAF3-deficient fibroblasts are defective in their type I IFN response to direct infection with vesicular stomatitis virus, indicating that TRAF3 is also an important component of TLR-independent viral recognition pathways. Our data demonstrate that TRAF3 is a major regulator of type I IFN production and the innate antiviral response.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

11 Bio Entities

Trail: Publication

0 Expression