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Protein Kinase-Regulated Inwardly Rectifying Anion and Organic Osmolyte Channels in Malaria-Infected Erythrocytes

机译:疟疾感染的红细胞中蛋白激酶调节的内向整流阴离子和有机渗透液通道

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The intraerythrocytic amplification of the malaria parasite Plasmodium falciparum induces new pathways ofsolute permeability in the host cell's membrane. These pathways play a pivotal role in parasite development by supplyingthe parasite with nutrients, disposing of the parasite's metabolic waste and organic osmolytes, and adapting the host'selectrolyte composition to the parasite's needs. During the last ten years, electrophysiological investigations stronglysupported earlier evidence obtained by transport and pharmacological studies that this new permeability pathway, whichis induced by the parasite in the host cell membrane, is constituted by anion-selective channels. This review surveys theevidences acquired using the patch-clamp technique and discuss the hypothesis that protein kinase A is an effector of thesignalling pathway leading to the activation of endogenous channels upon infection.
机译:疟原虫恶性疟原虫的红细胞内扩增在宿主细胞膜上诱导了溶质通透性的新途径。这些途径通过为寄生虫提供营养,处理寄生虫的代谢废物和有机渗透物,以及使宿主的电解质组成适应寄生虫的需要,在寄生虫的发展中发挥关键作用。在过去的十年中,电生理学研究强烈支持通过运输和药理学研究获得的较早的证据,这种新的通透性途径是由宿主细胞膜中的寄生虫诱导的,是由阴离子选择性通道构成的。这篇综述调查了使用膜片钳技术获得的证据,并讨论了蛋白激酶A是导致感染后激活内源通道的信号传递途径的效应子的假设。

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