耶尔森菌感染
中文名称
通路描述
致病耶尔森菌通过III型分泌系统(T3SS)将毒力耶尔森菌外蛋白(Yops)注入宿主细胞以表达其致病性。通过YopT蛋白酶小GTP酶失活、YopE GTP酶激活蛋白和YpkA/YopO小GTPase结合GDP的小GTP酶 sequestration,耶尔森菌阻止其被吞噬细胞摄取并破坏actin细胞骨架。YopH磷酸酶通过去磷酸化关键宿主蛋白关闭吞噬作用,并抑制T细胞激活。耶尔森菌通过YopB/YopD激活经典和非经典炎症小体以及YopT/YopE介导的pyrin激活诱导巨噬细胞焦亡。这些效应被YopK和YopM所抵消。YopP/J属于泛素样蛋白半胱氨酸蛋白酶家族,并在Toll样受体4激活后同时靶向MAPK和NF-kappaB信号通路中的信号组分,以抑制促炎细胞因子的产生。
英文描述
Pathogenic Yersinia injects virulent Yersinia outer proteins (Yops) into the host cell through a type three secretion system (T3SS) to express its pathogenicity. Through inactivation of small GTPases by YopT protease, YopE GTPase-activating protein, and YpkA/YopO sequestration of GDP-bound small GTPases, Yersinia prevents its uptake by phagocytic cells and disrupts the actin cytoskeleton. YopH phosphatase shuts down phagocytosis by dephosphorylating key host proteins as well as suppresses T cell activation. Yersinia induces macrophage pyroptosis via YopB/YopD activation of canonical and noncanonical inflammasomes and YopT/YopE-mediated activation of pyrin. These effects are counteracted by YopK and YopM. YopP/J is a member of an ubiquitin-like protein cysteine protease family and simultaneously targets signaling components of the MAPK and NF-kappaB signaling pathways following activation of Toll-like receptor4 to inhibit production of proinflammatory cytokines.
所含基因
138 个基因
ACTB
ACTG1
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AKT1
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ARF6
ARHGEF1
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