Orth Kim
Department of Molecular Biology, 5323 Harry Hines Boulevard, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA.
Curr Opin Microbiol. 2002 Feb;5(1):38-43. doi: 10.1016/s1369-5274(02)00283-7.
The Yersinia virulence factor YopJ inhibits the host immune response and induces apoptosis by blocking multiple signaling pathways, including the MAPK and NFkappaB pathways in the infected cell. YopJ is a cysteine protease that cleaves a reversible post-translational modification in the form of ubiquitin or a ubiquitin-like protein. Homologues of YopJ are expressed in animal and plant pathogens, as well as a plant symbiont, suggesting a universal mechanism of regulating or modulating a variety of signaling pathways. The ability of YopJ to block the innate immune response, its activity as a ubiquitin-like protein protease and its activity with respect to mammalian signalling pathways are discussed in this review.
耶尔森氏菌毒力因子YopJ通过阻断包括感染细胞中的丝裂原活化蛋白激酶（MAPK）和核因子κB（NFκB）途径在内的多种信号通路，抑制宿主免疫反应并诱导细胞凋亡。YopJ是一种半胱氨酸蛋白酶，可切割泛素或类泛素蛋白形式的可逆翻译后修饰。YopJ的同源物在动物和植物病原体以及一种植物共生体中表达，这表明存在调节或调控多种信号通路的普遍机制。本文综述了YopJ阻断天然免疫反应的能力、其作为类泛素蛋白蛋白酶的活性以及其对哺乳动物信号通路的活性。
