Protein lipidation, the covalent attachment of a lipid moiety to a target protein, plays a critical role in many cellular processes in eukaryotic cells. Bacterial pathogens secrete various effectors to subvert the host signaling pathway as a mechanism of microbial pathogenesis. An increasing number of effectors from diverse bacterial pathogens function as cysteine proteases to cause irreversible delipidation of host lipidated proteins. This in turn results in disruption of crucial lipidation-mediated host signal transduction, thereby enabling pathogen survival and replication. In this review, we discuss the role of the bacterial effectors in interactions with the host and highlight our knowledge of irreversible host delipidation, with a focus on the common concerted biochemical mechanisms of the bacterial effectors.

蛋白质脂化，即脂质部分与靶蛋白的共价连接，在真核细胞的许多细胞过程中起着关键作用。细菌病原体分泌各种效应物来破坏宿主信号通路，作为微生物发病机制。越来越多的来自不同细菌病原体的效应物起半胱氨酸蛋白酶的作用，导致宿主脂化蛋白的不可逆脱脂。这反过来又会破坏关键的脂化介导的宿主信号转导，从而使病原体能够存活和复制。在这篇综述中，我们讨论了细菌效应子在与宿主相互作用中的作用，并强调了我们对不可逆宿主脱脂的了解，重点是细菌效应子的共同协调生化机制。