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Transport mechanisms at the malaria parasite-host cell interface

机译:疟疾寄生虫 - 宿主细胞接口的运输机制

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摘要

Obligate intracellular malaria parasites reside within a vacuolar compartment generated during invasion which is the principal interface between pathogen and host. To subvert their host cell and support their metabolism, these parasites coordinate a range of transport activities at this membrane interface that are critically important to parasite survival and virulence, including nutrient import, waste efflux, effector protein export, and uptake of host cell cytosol. Here, we review our current understanding of the transport mechanisms acting at the malaria parasite vacuole during the blood and liver-stages of development with a particular focus on recent advances in our understanding of effector protein translocation into the host cell by the Plasmodium Translocon of EXported proteins (PTEX) and small molecule transport by the PTEX membrane-spanning pore EXP2. Comparison to Toxoplasma gondii and other related apicomplexans is provided to highlight how similar and divergent mechanisms are employed to fulfill analogous transport activities.
机译:在侵袭期间产生的血管室内的血管室内留在侵入过程中,这是病原体和宿主之间的主要界面。为了颠覆他们的宿主细胞并支持其新陈代谢,这些寄生虫在该膜界面处协调一系列的运输活性,对于寄生物存活和毒力,包括营养进口,废物流出,效应蛋白出口和宿主细胞胞嘧啶的吸收是至关重要的。在这里,我们审查了目前了解在血液和肝脏静脉期间对疟疾寄生虫液泡的运输机制的理解,特别关注我们通过出口疟原虫的疟原虫对宿主细胞进行效应蛋白易位的最新进展蛋白质(PTEX)和PTEX膜跨越孔Exp2的小分子输送。提供与弓形虫贡献和其他相关ApiCoMplems的比较以突出如何采用类似和发散的机制来满足类似的运输活性。

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