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顶复门寄生虫如何进出细胞。

How apicomplexan parasites move in and out of cells.

机构信息

Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Ave, St. Louis, MO 63110, USA.

出版信息

Curr Opin Biotechnol. 2010 Oct;21(5):592-8. doi: 10.1016/j.copbio.2010.05.009. Epub 2010 Jun 25.

DOI:10.1016/j.copbio.2010.05.009
PMID:20580218
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2947570/
Abstract

Apicomplexan parasites utilize a unique form of 'gliding motility' to traverse across substrates, migrate through tissues, and invade into and finally egress from their vertebrate host cells. Parasite gliding relies on the treadmilling of surface adhesins linked to short actin filaments that are translocated rearward by stationary small myosin motors. New details reveal mechanistic insight into the coordinated release and processing of adhesins, the complexity of adhesin-substrate interactions, the regulation of the actin-myosin motor complex, and the formation of a novel junction at the host-parasite interface. These activities are carefully orchestrated to provide an efficient process for motility that is essential for parasite survival. The parasite-specific nature of many of these steps reveals several essential points that may be targeted for intervention.

摘要

顶复门寄生虫利用独特的“滑行运动”形式在基质上移动,在组织中迁移,侵入并最终离开其脊椎动物宿主细胞。寄生虫滑行依赖于与短肌动蛋白丝相连的表面黏附素的履带运动,这些肌动蛋白丝由固定的小肌球蛋白马达向后输送。新的细节揭示了黏附素释放和加工的协调机制、黏附素-基质相互作用的复杂性、肌动球蛋白马达复合物的调节以及宿主-寄生虫界面上新型连接的形成。这些活动被精心协调,为运动提供了一个高效的过程,这对寄生虫的生存至关重要。许多这些步骤的寄生虫特异性揭示了几个可能作为干预目标的关键点。

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