Soulat Didier, Bauch Angela, Stockinger Silvia, Superti-Furga Giulio, Decker Thomas
Max F. Perutz Laboratories, University of Vienna, Austria.
FEBS Lett. 2006 Apr 17;580(9):2341-2346. doi: 10.1016/j.febslet.2006.03.057.
The mitochondria-associated adapter protein MAVS (also called IPS-1, VISA or CARDIF, designated MAVS for reasons of simplicity in our manuscript) relays signals from cytoplasmic sensors of viral RNA to the IRF3 kinase complex and the interferon-beta (IFN-beta) gene. Using siRNA-mediated knock-down in macrophages we show that IFN-beta synthesis in response to transfected, intracellular double-stranded RNA (dsRNA), a pathogen-associated molecular pattern of viruses, is decreased in absence of MAVS. By contrast, the Gram-positive bacterium Listeria monocytogenes targets the IFN-beta gene without detectable MAVS requirement. The data show that MAVS is not a central adapter protein for all cytoplasmic pathogen sensors that stimulate IFN-beta synthesis.
线粒体相关衔接蛋白MAVS（也称为IPS-1、VISA或CARDIF，在我们的稿件中为简便起见指定为MAVS）将病毒RNA的细胞质传感器发出的信号传递给IRF3激酶复合物和干扰素-β（IFN-β）基因。我们利用巨噬细胞中siRNA介导的敲低实验表明，在缺乏MAVS的情况下，对转染的细胞内双链RNA（dsRNA，一种病毒病原体相关分子模式）产生反应时，IFN-β的合成减少。相比之下，革兰氏阳性菌单核细胞增生李斯特菌靶向IFN-β基因，而无需检测到MAVS。数据表明，MAVS并非所有刺激IFN-β合成的细胞质病原体传感器的核心衔接蛋白。
