北京大學(xué)顧軍課題組的最新研究論文“Inhibition of RIG-I/MDA5 dependent antiviral response by gC1qR at mitochondria”發(fā)表在2009年美國(guó)科學(xué)院院刊（PNAS）上,。
RIG-I是近年來發(fā)現(xiàn)的抗病毒基因,，該基因產(chǎn)物可以作為RNA病毒的胞內(nèi)受體，激活抗病毒的信號(hào)通路，誘導(dǎo)β-干擾素的表達(dá),。顧軍老師實(shí)驗(yàn)室的研究發(fā)現(xiàn),，病毒的雙鏈RNA可以結(jié)合宿主細(xì)胞的gC1qR (補(bǔ)體蛋白C1q的受體),。這種結(jié)合引起gC1qR向線粒體的轉(zhuǎn)位,，轉(zhuǎn)位的gC1qR與線粒體定位蛋白MAVS結(jié)合。MAVS是RIG-I下游的接頭蛋白,，傳遞RIG-I的抗病毒信號(hào),。gC1qR與MAVS的結(jié)合，阻斷了RIG-I的信號(hào)通路,，從而抑制β-干擾素的誘導(dǎo)表達(dá),，抑制了細(xì)胞的抗病毒作用。這一研究不僅完整揭示了gC1qR新的作用機(jī)制，同時(shí)也是第一次揭示了病毒利用宿主的內(nèi)源蛋白逃逸機(jī)體免疫的另一種策略,，這一結(jié)果為今后的抗病毒研究提供了新的科學(xué)依據(jù),。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
