一个阿斯巴提尔蛋白酶将疟疾效应蛋白引导到宿主细胞中
Justin A Boddey1, Anthony N Hodder, Svenja Günther
1The Walter and Eliza Hall Institute of Medical Research, Melbourne 3052, Australia.
Nature
|February 5, 2010
概括
疟疾寄生虫Plasmodium falciparum使用一个特定的模式出口蛋白质. 研究人员确定了等离子素V (PMV) 作为切割这种基因所必需的蛋白酶,使寄生虫能够存活,并提供了一个新的治疗点.
科学领域:
- 分子寄生虫学 分子寄生虫学
- 传染性疾病 传染性疾病
- 红细胞生物学 红细胞生物学
背景情况:
- 疟原虫 (Plasmodium falciparum) 通过重塑受感染的红细胞,导致严重的疟疾.
- 寄生虫的生存取决于在真空层之外输出效应蛋白.
- 出口的蛋白质共享一个被保存的 pentameric 动图 (RxLxE/Q/D),被一个未知的蛋白酶分裂.
研究的目的:
- 确定负责在Plasmodium falciparum中切割pentameric出口基因的蛋白酶.
- 阐明这种蛋白酶在红细胞重塑和寄生虫毒性中的作用.
主要方法:
- 生物化学测试以确定蛋白酶活性.
- 这是对Plasmodium falciparum的基因操纵.
- 蛋白质出口和N终端加工的分析.
主要成果:
- 塑素V (PMV),一种ER-居民的酸蛋白酶,被确定为负责的蛋白酶.
- PMV将RxLxE/Q/D图形切割出来,显示出N端出口信号 (xE/Q/D).
- PMV活动对于蛋白质出口至关重要,并且与其他关键的出口事件相关,与信号酶处理不同.
结论:
- 血素V对于Plasmodium falciparum效应蛋白在红细胞中的输出至关重要.
- 以PMV为媒介的裂变是寄生虫毒性的一个关键步骤.
- PMV代表了疟疾治疗的新型治疗标.
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