Four miR-27a binding sites were recognized in the MAVS 3'UTR, and treatment of miR-27a inhibited MAVS expression and promoted the replication of the vesicular stomatitis virus (VSV).
We previously demonstrated that the serine/threonine kinase IKKε is recruited to the C-terminal region of MAVS following Sendai or vesicular stomatitis virus (VSV) infection, mediated by Lys63-linked polyubiquitination of MAVS at Lys500, resulting in inhibition of downstream IFN signaling (Paz et al, Mol Cell Biol, 2009).