Making Contact: VAP Targeting by Intracellular Pathogens.

Contact (Thousand Oaks (Ventura County, Calif.)) Pub Date : 2018-05-17 eCollection Date: 2018-01-01 DOI:10.1177/2515256418775512
Rebecca Stanhope, Isabelle Derré
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引用次数: 9

Abstract

In naïve cells, the endoplasmic reticulum (ER) and the ER-resident Vesicle-associated membrane protein-Associated Proteins (VAP) are common components of sites of membrane contacts that mediate the nonvesicular transfer of lipids between organelles. There is increasing recognition that the hijacking of VAP by intracellular pathogens is a novel mechanism of host-pathogen interaction. Here, we summarize our recent findings showing that the Chlamydia inclusion membrane protein IncV tethers the ER to the inclusion membrane by binding to VAP via the molecular mimicry of two eukaryotic FFAT motifs. We extend the discussion to other microorganisms that have evolved similar mechanisms.

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接触:细胞内病原体靶向VAP。
在幼稚细胞中,内质网(ER)和内质网驻留的小泡相关膜蛋白相关蛋白(VAP)是介导细胞器之间脂质非小泡转移的膜接触位点的常见组成部分。人们越来越认识到,细胞内病原体劫持VAP是一种新的宿主-病原体相互作用机制。在这里,我们总结了我们最近的发现,即衣原体包涵体膜蛋白IncV通过两个真核FFAT基序的分子模拟与VAP结合,将ER连接到包涵体膜上。我们将讨论扩展到其他进化出类似机制的微生物。
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