Research Project
Grant-in-Aid for Research Activity Start-up
Retroviruses have evolved effective strategies to evade the host immune response thereby allowing continuous and efficient viral replication. We investigated the action of the HIV-1 protease on the modification of immune signaling. Using the wheat cell-free protein synthesis system and the amplified luminescent proximity homogeneous assay (AlphaScreen), we found that TANK-binding kinase 1 (TBK1) is a substrate for HIV-1 protease. We further revealed that HIV-1 protease cleaved the C-terminal domain of TBK1 and this effect can impair the function of TBK1 for the phosphorylation of IRF-3 and the transactivation of INFβ promoter. These results together indicate that HIV-1 protease may disrupt the innate immune signaling via targeting TBK1 leading to escape from the anti-viral immune response.
All 2012 2011 Other
All Presentation (5 results)
