北京大学顾军课题组的最新研究论文“Inhibition of RIG-I/MDA5 dependent antiviral response by gC1qR at mitochondria”发表在2009年美国科学院院刊（PNAS）上。
RIG-I是近年来发现的抗病毒基因，该基因产物可以作为RNA病毒的胞内受体，激活抗病毒的信号通路，诱导β-干扰素的表达。顾军老师实验室的研究发现，病毒的双链RNA可以结合宿主细胞的gC1qR (补体蛋白C1q的受体)。这种结合引起gC1qR向线粒体的转位，转位的gC1qR与线粒体定位蛋白MAVS结合。MAVS是RIG-I下游的接头蛋白，传递RIG-I的抗病毒信号。gC1qR与MAVS的结合，阻断了RIG-I的信号通路，从而抑制β-干扰素的诱导表达，抑制了细胞的抗病毒作用。这一研究不仅完整揭示了gC1qR新的作用机制，同时也是第一次揭示了病毒利用宿主的内源蛋白逃逸机体免疫的另一种策略，这一结果为今后的抗病毒研究提供了新的科学依据。（生物谷Bioon.com）
生物谷推荐原始出处：
PNAS January 21, 2009, doi: 10.1073/pnas.0811029106
Inhibition of RIG-I and MDA5-dependent antiviral response by gC1qR at mitochondria
Lijuan Xu1, Nengming Xiao1,2, Feng Liu, Hongwei Ren and Jun Gu3
National Key Laboratory of Protein Engineering and Plant Gene Engineering, College of Life Sciences, Peking University, Beijing, China
1L.X. and N.X. contributed equally to this work. (received for review October 31, 2008)
Abstract
gC1qR is one of the C1q receptors implicated in the regulation of innate and adaptive immunity. We found that gC1qR inhibits RIG-I and MDA5-dependent antiviral signaling. Double stranded RNA and virus trigger the translocation of gC1qR to the mitochondrial outer membrane leading to the interaction of gC1qR with the RIG-I and MDA5 adaptor, VISA/MAVS/IPS-1/Cardif. The interaction of gC1qR with VISA/MAVS/IPS-1/Cardif at mitochondria results in the disruption of RIG-I and MDA5 signaling and the promotion of virus replication. Knockdown of endogenous gC1qR enhances RIG-I-dependent antiviral signaling, and augments the inhibition of virus proliferation. Therefore, gC1qR is a physiological inhibitor of the RIG-I and MDA5-mediated antiviral signaling pathway. These data uncover a new viral mechanism used to negatively control antiviral signaling in host cells.
