疟原虫为什么会增加宿主红细胞的通透性？
Why do malaria parasites increase host erythrocyte permeability?
机构信息
Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA.
出版信息
Trends Parasitol. 2014 Mar;30(3):151-9. doi: 10.1016/j.pt.2014.01.003. Epub 2014 Feb 5.
Abstract
Malaria parasites increase erythrocyte permeability to diverse solutes including anions, some cations, and organic solutes, as characterized with several independent methods. Over the past decade, patch-clamp studies have determined that the permeability results from one or more ion channels on the infected erythrocyte host membrane. However, the biological role(s) served by these channels, if any, remain controversial. Recent studies implicate the plasmodial surface anion channel (PSAC) and a role in parasite nutrient acquisition. A debated alternative role in remodeling host ion composition for the benefit of the parasite appears to be nonessential. Because both channel activity and the associated clag3 genes are strictly conserved in malaria parasites, channel-mediated permeability is an attractive target for development of new therapies.
摘要
疟原虫增加红细胞对多种溶质的通透性，包括阴离子、一些阳离子和有机溶质，这可以通过几种独立的方法来表征。在过去的十年中，膜片钳研究已经确定，这种通透性是由感染红细胞宿主膜上的一个或多个离子通道引起的。然而，这些通道（如果有的话）所起的生物学作用仍然存在争议。最近的研究表明，疟原虫表面阴离子通道（PSAC）在寄生虫获取营养物质方面发挥作用。另一种有争议的替代作用是为寄生虫重塑宿主离子组成，但似乎并非必不可少。由于这两种通道活性和相关的 clag3 基因在疟原虫中都严格保守，因此通道介导的通透性是开发新疗法的一个有吸引力的靶点。
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2
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Cell Microbiol. 2013 Nov;15(11):1913-23. doi: 10.1111/cmi.12162. Epub 2013 Jul 19.
3
An epigenetic antimalarial resistance mechanism involving parasite genes linked to nutrient uptake.一种涉及寄生虫与营养摄取相关基因的表观遗传抗疟耐药机制。
J Biol Chem. 2013 Jul 5;288(27):19429-40. doi: 10.1074/jbc.M113.468371. Epub 2013 May 28.
4
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