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刚地弓形虫和疟原虫蛋白激酶:在入侵和宿主细胞重塑中的作用。

Toxoplasma and Plasmodium protein kinases: roles in invasion and host cell remodelling.

机构信息

David H. Koch Institute for Integrative Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

出版信息

Int J Parasitol. 2012 Jan;42(1):21-32. doi: 10.1016/j.ijpara.2011.11.007. Epub 2011 Dec 4.

DOI:10.1016/j.ijpara.2011.11.007
PMID:22154850
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3428259/
Abstract

Some apicomplexan parasites have evolved distinct protein kinase families to modulate host cell structure and function. Toxoplasma gondii rhoptry protein kinases and pseudokinases are involved in virulence and modulation of host cell signalling. The proteome of Plasmodium falciparum contains a family of putative kinases called FIKKs, some of which are exported to the host red blood cell and might play a role in erythrocyte remodelling. In this review we will discuss kinases known to be critical for host cell invasion, intracellular growth and egress, focusing on (i) calcium-dependent protein kinases and (ii) the secreted kinases that are unique to Toxoplasma (rhoptry protein kinases and pseudokinases) and Plasmodium (FIKKs).

摘要

一些顶复门寄生虫已经进化出独特的蛋白激酶家族来调节宿主细胞的结构和功能。刚地弓形虫的泡颈蛋白激酶和拟激酶参与了毒力和宿主细胞信号转导的调节。疟原虫的蛋白质组包含一个称为 FIKKs 的假定激酶家族,其中一些被输出到宿主红细胞,并可能在红细胞重塑中发挥作用。在这篇综述中,我们将讨论已知对宿主细胞入侵、细胞内生长和逸出至关重要的激酶,重点讨论(i)钙依赖性蛋白激酶和(ii)刚地弓形虫(泡颈蛋白激酶和拟激酶)和疟原虫(FIKKs)所特有的分泌激酶。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c91/3428259/1a9d11d04e65/nihms342442f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c91/3428259/21b8c0ba7b15/nihms342442f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c91/3428259/1a9d11d04e65/nihms342442f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c91/3428259/21b8c0ba7b15/nihms342442f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c91/3428259/1a9d11d04e65/nihms342442f2.jpg

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本文引用的文献

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Global kinomic and phospho-proteomic analyses of the human malaria parasite Plasmodium falciparum.全球人类疟原虫恶性疟原虫的蛋白质组学和磷酸化蛋白质组学分析。
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Toxoplasma gondii rhoptry kinase ROP16 activates STAT3 and STAT6 resulting in cytokine inhibition and arginase-1-dependent growth control.刚地弓形虫棒状体蛋白激酶 ROP16 激活 STAT3 和 STAT6,导致细胞因子抑制和依赖精氨酸酶-1 的生长控制。
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A conserved non-canonical motif in the pseudoactive site of the ROP5 pseudokinase domain mediates its effect on Toxoplasma virulence.ROP5 假激酶结构域假活性位点中的一个保守非典型模体介导其对弓形虫毒力的影响。
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Toxoplasma polymorphic effectors determine macrophage polarization and intestinal inflammation.刚地弓形虫多态效应物决定巨噬细胞极化和肠道炎症。
Cell Host Microbe. 2011 Jun 16;9(6):472-83. doi: 10.1016/j.chom.2011.04.015.
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Virulence differences in Toxoplasma mediated by amplification of a family of polymorphic pseudokinases.家族中一系列多态假激酶的扩增导致弓形虫毒力差异。
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