Arp2/3-mediated actin-based motility: a tail of pathogen abuse.

Arp2/3-mediated actin-based motility: a tail of pathogen abuse.
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ARP2/3介导的基于肌动蛋白的运动:病原体滥用的尾巴。

DOI:
10.1016/j.chom.2013.08.011
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发表时间:
2013-09-11
影响因子:
30.3
通讯作者:
Way M
Way M
中科院分区:
医学1区
文献类型:
--
作者:
Welch MD;Way M

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细胞内病原体已经发展出复杂的机制来利用它们不情愿的宿主的不同细胞系统来促进它们的进入、复制和存活。特别是,各种各样的细菌和病毒已经进化出独特的策略来利用Arp 2/3介导的肌动蛋白聚合的力量来增强它们的细胞间传播。在这篇综述中,我们将讨论如何研究这些病原体已经彻底改变了我们的Arp 2/3依赖的肌动蛋白组装的分子理解,并揭示了调节细胞中肌动蛋白组装的关键信号通路。对已知和新出现的病原体的进一步研究无疑将继续增强我们对肌动蛋白细胞骨架在发病过程中的作用的理解。此外,回顾过去的20年,如果未来对微生物-宿主相互作用的分析没有继续发现调节肌动蛋白组装和动力学的新机制,以及肌动蛋白意想不到的细胞功能,那将是令人惊讶的。
Intracellular pathogens have developed elaborate mechanisms to exploit the different cellular systems of their unwilling hosts to facilitate their entry, replication and survival. In particular, a diverse range of bacteria and viruses have evolved unique strategies to harness the power of Arp2/3-mediated actin polymerization to enhance their cell-to-cell spread. In this review, we discuss how studying these pathogens has revolutionized our molecular understanding of Arp2/3-dependent actin assembly, and revealed key signalling pathways regulating actin assembly in cells. Further studies with known and newly emerging pathogens will undoubtedly continue to enhance our understanding of the role of the actin cytoskeleton during pathogenesis. Moreover, looking back over the last 20 years, it would be surprising if future analyses of microbe-host interactions did not continue to uncover new mechanisms regulating actin assembly and dynamics, as well as unexpected cellular functions for actin.
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