The mechanism of erythrocyte invasion by the malarial parasite, Plasmodium falciparum

被引:27
作者
Farrow, Rachel E. [1 ]
Green, Judith [1 ]
Katsimitsoulia, Zoe [1 ]
Taylor, William R. [1 ]
Holder, Anthony A. [1 ]
Molloy, Justin E. [1 ]
机构
[1] MRC Natl Inst Med Res, London NW7 1AA, England
基金
英国医学研究理事会;
关键词
Malaria; Plasmodium; MyoA; Myosin; Invasion; HOST-CELL INVASION; GONDII MYOSIN-A; TOXOPLASMA-GONDII; APICOMPLEXAN PARASITES; ACTIN POLYMERIZATION; GLIDING MOTILITY; MOVING JUNCTION; PROTEIN-KINASE; COMPLEX; MOTOR;
D O I
10.1016/j.semcdb.2011.09.022
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Plasmodium falciparum is the most virulent causative agent of malaria in man accounting for 80% of all malarial infections and 90% of the one million annual deaths attributed to malaria. P. falciparum is a unicellular, Apicomplexan parasite, that spends part of its lifecycle in the mosquito and part in man and it has evolved a special form of motility that enables it to burrow into animal cells, a process termed "host cell invasion". The acute, life threatening, phase of malarial infection arises when the merozoite form of the parasite undergoes multiple cycles of red blood cell invasion and rapid proliferation. Here, we discuss the molecular machinery that enables malarial parasites to invade red blood cells and we focus particularly on the ATP-driven acto-myosin motor that powers invasion. Crown Copyright (C) 2011 Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:953 / 960
页数:8
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