TY - JOUR
T1 - The mitochondrial targeting chaperone 14-3-3ε regulates a RIG-I translocon that mediates membrane association and innate antiviral immunity
AU - Liu, Helene Minyi
AU - Loo, Yueh Ming
AU - Horner, Stacy M.
AU - Zornetzer, Gregory A.
AU - Katze, Michael G.
AU - Gale, Michael
PY - 2012/5/17
Y1 - 2012/5/17
N2 - RIG-I is a cytosolic pathogen recognition receptor that initiates immune responses against RNA viruses. Upon viral RNA recognition, antiviral signaling requires RIG-I redistribution from the cytosol to membranes where it binds the adaptor protein, MAVS. Here we identify the mitochondrial targeting chaperone protein, 14-3-3ε, as a RIG-I-binding partner and essential component of a translocation complex or "translocon" containing RIG-I, 14-3-3ε, and the TRIM25 ubiquitin ligase. The RIG-I translocon directs RIG-I redistribution from the cytosol to membranes where it mediates MAVS-dependent innate immune signaling during acute RNA virus infection. 14-3-3ε is essential for the stable interaction of RIG-I with TRIM25, which facilitates RIG-I ubiquitination and initiation of innate immunity against hepatitis C virus and other pathogenic RNA viruses. Our results define 14-3-3ε as a key component of a RIG-I translocon required for innate antiviral immunity.
AB - RIG-I is a cytosolic pathogen recognition receptor that initiates immune responses against RNA viruses. Upon viral RNA recognition, antiviral signaling requires RIG-I redistribution from the cytosol to membranes where it binds the adaptor protein, MAVS. Here we identify the mitochondrial targeting chaperone protein, 14-3-3ε, as a RIG-I-binding partner and essential component of a translocation complex or "translocon" containing RIG-I, 14-3-3ε, and the TRIM25 ubiquitin ligase. The RIG-I translocon directs RIG-I redistribution from the cytosol to membranes where it mediates MAVS-dependent innate immune signaling during acute RNA virus infection. 14-3-3ε is essential for the stable interaction of RIG-I with TRIM25, which facilitates RIG-I ubiquitination and initiation of innate immunity against hepatitis C virus and other pathogenic RNA viruses. Our results define 14-3-3ε as a key component of a RIG-I translocon required for innate antiviral immunity.
UR - http://www.scopus.com/inward/record.url?scp=84861181618&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84861181618&partnerID=8YFLogxK
U2 - 10.1016/j.chom.2012.04.006
DO - 10.1016/j.chom.2012.04.006
M3 - Article
C2 - 22607805
AN - SCOPUS:84861181618
SN - 1931-3128
VL - 11
SP - 528
EP - 537
JO - Cell Host and Microbe
JF - Cell Host and Microbe
IS - 5
ER -
