Nutrition, Inflammation et Dysfonction de l'Axe Intestin-Cerveau, Institut National de la Santé et de la Recherche Médicale (INSERM) U1073, Normandie Université, Université de Rouen, Rouen, France.
Unité des Interactions Bactéries-Cellules, Institut Pasteur, INSERM U604, Institut National de la Recherche Agronomique (INRA) USC2020, Paris, France.
Trends Cell Biol. 2018 Nov;28(11):926-940. doi: 10.1016/j.tcb.2018.07.005. Epub 2018 Aug 11.
Manipulation of host protein post-translational modifications (PTMs) is used by various pathogens to interfere with host cell functions. Among these modifications, ubiquitin (UBI) and ubiquitin-like proteins (UBLs) constitute key targets because they are regulators of pathways essential for the host cell. In particular, these PTM modifiers control pathways that have been described as crucial for infection such as pathogen entry, replication, propagation, or detection by the host. Although bacterial pathogens lack eucaryotic-like UBI or UBL systems, many of them produce proteins that specifically interfere with these host PTMs during infection. In this review we discuss the different mechanisms used by bacteria to interfere with host UBI and the two UBLs, SUMO and NEDD8.
宿主蛋白翻译后修饰(PTMs)的操纵被各种病原体用于干扰宿主细胞功能。在这些修饰中,泛素(UBI)和泛素样蛋白(UBLs)是关键靶标,因为它们是宿主细胞必需途径的调节剂。特别是,这些 PTM 修饰物控制着已被描述为感染关键的途径,如病原体进入、复制、繁殖或宿主检测。尽管细菌病原体缺乏真核生物样 UBI 或 UBL 系统,但它们中的许多产生的蛋白质在感染过程中专门干扰这些宿主 PTMs。在这篇综述中,我们讨论了细菌用于干扰宿主 UBI 和两种 UBLs(SUMO 和 NEDD8)的不同机制。