恶性疟原虫
顶端体
生物
配子体
运输机
疟原虫(生命周期)
细胞生物学
重组DNA
寄生虫寄主
生物化学
转运蛋白
锌
胞浆
病毒学
疟疾
顶复亚门
基因
化学
酶
免疫学
有机化学
万维网
计算机科学
作者
D. L. Shrivastava,A. Jha,Rajlakshmi Kabrambam,Jyoti Vishwakarma,Kalyan Mitra,Ravishankar Ramachandran,Saman Habib
出处
期刊:ACS Infectious Diseases
[American Chemical Society]
日期:2024-01-01
卷期号:10 (1): 155-169
标识
DOI:10.1021/acsinfecdis.3c00426
摘要
Replication of the malarial parasite in human erythrocytes requires massive zinc fluxes, necessitating the action of zinc transporters across the parasite plasma and organellar membranes. Although genetic knockout studies have been conducted on a few "orphan" zinc transporters in Plasmodium spp., none of them have been functionally characterized. We used the recombinant Plasmodium falciparum Zrt-/Irt-like protein (PfZIP1) and specific antibodies generated against it to explore the subcellular localization, function, metal-ion selectivity, and response to cellular zinc levels. PfZIP1 expression was enhanced upon the depletion of cytosolic Zn2+. The protein transitioned from the processed to unprocessed form through blood stages, localizing to the apicoplast in trophozoites and to the parasite plasma membrane in schizonts and gametocytes, indicating stage-specific functional role. The PfZIP1 dimer mediated Zn2+ influx in proteoliposomes. It exhibited preferential binding to Zn2+ compared to Fe2+, with the selectivity for zinc being driven by a C-terminal histidine-rich region conserved only in primate-infecting Plasmodium species.
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