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人类红细胞感染疟原虫后的重塑及其对 PHIST 蛋白的影响。

Remodeling of human red cells infected with Plasmodium falciparum and the impact of PHIST proteins.

机构信息

Molecular Biology Division, National Institute of Malaria Research, New Delhi 110077, India.

出版信息

Blood Cells Mol Dis. 2013 Oct;51(3):195-202. doi: 10.1016/j.bcmd.2013.06.003. Epub 2013 Jul 21.

DOI:10.1016/j.bcmd.2013.06.003
PMID:23880461
Abstract

In an infected erythrocyte (iRBC), renovation and decoration are crucial for malarial parasite survival, pathogenesis and reproduction. Host cell remodeling is mediated by an array of diverse parasite-encoded export proteins that traffic within iRBC. These remodeling proteins extensively modify the membrane and cytoskeleton of iRBC and help in formation of parasite-induced novel organelles such as 'Maurer's Cleft (MC), tubulovesicular network (TVN) and parasitophorous vacuole membrane (PVM) inside the iRBC. The genome sequence of Plasmodium falciparum shows expansion of export proteins, which suggests a complex requirement of these export proteins for specific pathogenesis and erythrocyte remodeling. Plasmodium helical intersperse sub-telomeric (PHIST) is a family of seventy-two small export proteins and many of its recently discovered functional characteristics suggest an intriguing putative role in modification of an iRBC. This review highlights the recent advances in parasite genomics, proteomics, and cell biology studies unraveling the host cell modification; providing a speculation on the impact of PHIST proteins in modification of the iRBC.

摘要

在感染的红细胞(iRBC)中,改造和装饰对于疟原虫的生存、发病机制和繁殖至关重要。宿主细胞的重塑是由一系列多样化的寄生虫编码的输出蛋白介导的,这些蛋白在 iRBC 内运输。这些重塑蛋白广泛修饰 iRBC 的膜和细胞骨架,并有助于形成寄生虫诱导的新型细胞器,如“ Maurer 的裂隙(MC)”、管状囊泡网络(TVN)和 iRBC 内的寄生泡膜(PVM)。疟原虫 falciparum 的基因组序列显示出输出蛋白的扩张,这表明这些输出蛋白对特定的发病机制和红细胞重塑有复杂的要求。疟原虫螺旋间端粒区(PHIST)是一个由七十二个小输出蛋白组成的家族,其最近发现的许多功能特征表明,它在修饰 iRBC 方面具有有趣的潜在作用。这篇综述强调了寄生虫基因组学、蛋白质组学和细胞生物学研究的最新进展,揭示了宿主细胞的修饰;并对 PHIST 蛋白在修饰 iRBC 方面的影响进行了推测。

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