Reorganization of the host cell Crk(L)-PI3 kinase signaling complex by the influenza A virus NS1 protein.

摘要: Abstract The non-structural protein-1 (NS1) of influenza A virus binds the p85β subunit phosphoinositide 3-kinase (PI3K) to induce PI3K activity in infected cells. Some strains encode NS1 containing a motif that tightly SH3 domain cellular adapter proteins Crk and CrkL potentiate NS1-induced activation. Here we show this potentiation involves reorganization natural CrkL–p85β complex into novel trimeric where serves as bridging factor. Of note, lack binding capacity can also associate with CrkL, but less stable mediated by p85β. data presented here establish general host cell cofactors NS1, enhanced activation binding-competent variants is more efficient tethering NS1–PI3K complex.