A plant-like kinase in Plasmodium falciparum regulates parasite egress from erythrocytes.
A plant-like kinase in Plasmodium falciparum regulates parasite egress from erythrocytes.
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DOI：
10.1126/science.1188191
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发表时间：
2010-05-14
期刊：
影响因子：
--
通讯作者：
Duraisingh MT
中科院分区：
文献类型：
--
作者：
Dvorin JD;Martyn DC;Patel SD;Grimley JS;Collins CR;Hopp CS;Bright AT;Westenberger S;Winzeler E;Blackman MJ;Baker DA;Wandless TJ;Duraisingh MT
临床疟疾与人体红细胞中疟原虫寄生虫的增殖有关。寄生虫从红细胞排出和侵入红细胞的协调过程是快速和严格调节的。在这里，我们发现，植物样钙依赖性蛋白激酶PfCDPK5，这是恶性疟原虫的侵入裂殖子形式表达，是至关重要的出口。尽管出口蛋白酶和入侵配体正常成熟，但PfCDPK5缺陷的寄生虫作为具有完整膜的成熟寄生虫被捕。裂殖子从停滞的红细胞中物理释放出来，能够侵入新的红细胞，分离出出和侵入的途径。该阻滞是cGMP依赖性蛋白激酶（PfPKG）功能的下游，并且独立于蛋白酶加工。因此，PfCDPK5在疟疾复制的血液阶段中发挥重要作用。
Clinical malaria is associated with the proliferation of Plasmodium parasites in human erythrocytes. The coordinated processes of parasite egress from and invasion into erythrocytes are rapid and tightly regulated. Here we found that the plant-like calcium-dependent protein kinase PfCDPK5, which is expressed in invasive merozoite forms of Plasmodium falciparum, was critical for egress. Parasites deficient in PfCDPK5 arrested as mature schizonts with intact membranes, despite normal maturation of egress proteases and invasion ligands. Merozoites physically released from stalled schizonts were capable of invading new erythrocytes, separating the pathways of egress and invasion. The arrest was downstream of cGMP-dependent protein kinase (PfPKG) function and independent of protease processing. Thus PfCDPK5 plays an essential role of PfCDPK5 during the blood-stage of malaria replication.
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影响因子：
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作者：
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通讯作者：
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影响因子：
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