TRAF3IP3 mediates the recruitment of TRAF3 to MAVS for antiviral innate immunity

ABSTRACT: RIG-I-MAVS antiviral signaling represents an important pathway to stimulate interferon production and confer innate immunity to the host. Upon binding to viral RNA and Riplet-mediated polyubiquitination, RIG-I promotes prion-like aggregation and activation of MAVS. MAVS subsequently induces interferon production by activating two signaling pathways mediated by TBK1-IRF3 and IKK-NF-?B respectively. However, the mechanism underlying the activation of MAVS downstream pathways remains elusive. Here we demonstrated that activation of TBK1-IRF3 by MAVS-Region III depends on its multimerization state and identified TRAF3IP3 as a critical regulator for the downstream signaling. In response to virus infection, TRAF3IP3 is accumulated on mitochondria and thereby facilitate the recruitment of TRAF3 t

SUBMITTER: Dr. Fajian Hou 

PROVIDER: S-SCDT-EMBOJ-2019-102075 | biostudies-other |

REPOSITORIES: biostudies-other