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氯霉素和四环素发挥活性的一个途径就是阻碍细菌蛋白质的分泌,其分泌功能是由其氨基端的信号序列决定的,该序列能将蛋白质引导到由SecY,E,G和A组成的转运蛋白复合体上。蛋白的转运还取决于融合蛋白的折叠特点,蛋白质转运到周质后的错误折叠可导致毒素聚集体形成,快速折叠还会使转运复合体发生拥堵,使所有的蛋白质分泌都受到抑制,导致细胞死亡。抗生素氯霉素和四环素处理细菌后会导致转运复合体中SecY的降解,造成致命的蛋白拥堵。现就抗生素氯霉素和四环素的干扰细菌蛋白质合成的作用机制以及导致SecY的降解来发挥阻碍细菌蛋白质分泌活性的一个新模式进行概述,以期为探讨新的靶向细菌的治疗方法提供科学依据。
One of the ways in which chloramphenicol and tetracycline exert their activity is to hinder the secretion of bacterial proteins whose secretory function is dictated by the amino-terminal signal sequence that directs the protein to the transporter complex composed of SecY, E, G and A Body. Protein transport also depends on the folding characteristics of the fusion protein. Misfolding of the protein after transport to the periplasm can lead to the formation of toxoid aggregates. Rapid folding can also congest the transporter complex, inhibiting the secretion of all proteins, resulting in cells death. Antibiotics Chloramphenicol and tetracycline treatment of bacteria cause degradation of SecY in the transporter complex, resulting in fatal protein congestion. A new model of antibacterial activity of chloramphenicol and tetracycline interfering with bacterial protein synthesis and the degradation of SecY are presented to provide a scientific basis for exploring new therapeutic approaches targeting bacteria.