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Antimicrobial resistance

Reactome ID: R-HSA-9913143

中文名称

缺陷的 FV 变体在 R334 处的切割

通路描述

在正常的生理条件下,激活的蛋白 C (APC) 通过切割因子 Va (FVa) 在残基 R534 和 R334 处,从而防止过量的凝血形成。该 Reactome 事件描述了两个错义变体 FV R334T (FV Cambridge) 和 FV I387T (FV Liverpool),它们干扰 APC 介导的 R334 切割。这种受损的 FVa 蛋白酶解导致 FVa 的凝血活性延长,携带这两种突变个体的静脉血栓栓塞 (VTE) 风险可能增加 (Williamson D et al., 1998; Franco RF et al., 1998; Norström E et al., 2002; Mumford AD et al., 2003; Steen M et al., 2004; 综述由 Moore GW et al., 2023)。
英文描述
Antimicrobial resistance Resistance of microorganisms (bacteria, viruses, parasites) to antimicrobials is one of the most important public health problems. Infection with enterobacteria is treated with antibiotics from four groups (beta-lactams, aminoglycosides, tetracyclins and fluorquinolones). The main resistance mechanisms against these molecules are enzymatic degradation, efflux, inhibition of the drug's binding reaction, or usage of a back up pathway. Resistance against antiseptics and disinfectants is conferred by efflux proteins, biofilm formation or modification of targets (reviewed in Tong et al., 2021). Resistance mechanisms are either acquired by mutation, by horizontal gene transfer, or are already intrinsic to the organism. Participation of the organism in a consortium (like in biofilms) enables additional resistance mechanisms (reviewed in van Acker et al. 2014; van Acker & Coenye 2016; Alav et al., 2021; Aminov & Mackie 2007; Doi et al., 2016; Peterson & Kaur 2018; Urban-Chmiel et al., 2022).

所含基因

3 个基因