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本文引用的文献

1
Two Plasmodium rhomboid proteases preferentially cleave different adhesins implicated in all invasive stages of malaria.两种疟原虫类菱形蛋白酶优先切割与疟疾所有侵袭阶段相关的不同黏附素。
PLoS Pathog. 2006 Oct;2(10):e113. doi: 10.1371/journal.ppat.0020113.
2
Intramembrane proteolysis mediates shedding of a key adhesin during erythrocyte invasion by the malaria parasite.膜内蛋白水解作用介导疟原虫入侵红细胞过程中一种关键黏附素的脱落。
J Cell Biol. 2006 Sep 25;174(7):1023-33. doi: 10.1083/jcb.200604136.
3
A conserved region in the EBL proteins is implicated in microneme targeting of the malaria parasite Plasmodium falciparum.EBL蛋白中的一个保守区域与恶性疟原虫的微线体靶向有关。
J Biol Chem. 2006 Oct 20;281(42):31995-2003. doi: 10.1074/jbc.M606717200. Epub 2006 Aug 25.
4
Distinct mechanisms govern proteolytic shedding of a key invasion protein in apicomplexan pathogens.不同的机制控制着顶复门病原体中一种关键入侵蛋白的蛋白水解切割。
Mol Microbiol. 2005 Sep;57(5):1342-56. doi: 10.1111/j.1365-2958.2005.04772.x.
5
Rhomboid-like proteins in Apicomplexa: phylogeny and nomenclature.顶复门中类菱形蛋白:系统发育与命名
Trends Parasitol. 2005 Jun;21(6):254-8. doi: 10.1016/j.pt.2005.04.009.
6
A spatially localized rhomboid protease cleaves cell surface adhesins essential for invasion by Toxoplasma.一种在空间上定位的类菱形蛋白酶可切割对弓形虫入侵至关重要的细胞表面黏附素。
Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4146-51. doi: 10.1073/pnas.0407918102. Epub 2005 Mar 7.
7
Reconstitution of intramembrane proteolysis in vitro reveals that pure rhomboid is sufficient for catalysis and specificity.体外膜内蛋白水解的重组表明,纯菱形蛋白酶足以进行催化并具有特异性。
Proc Natl Acad Sci U S A. 2005 Feb 8;102(6):1883-8. doi: 10.1073/pnas.0408306102. Epub 2005 Jan 31.
8
Correlation of structural development and differential expression of invasion-related molecules in schizonts of Plasmodium falciparum.恶性疟原虫裂殖体结构发育与侵袭相关分子差异表达的相关性
Parasitology. 2004 Sep;129(Pt 3):273-87. doi: 10.1017/s0031182004005657.
9
Automatic and quantitative measurement of protein-protein colocalization in live cells.活细胞中蛋白质-蛋白质共定位的自动定量测量。
Biophys J. 2004 Jun;86(6):3993-4003. doi: 10.1529/biophysj.103.038422.
10
Allelic polymorphisms in apical membrane antigen-1 are responsible for evasion of antibody-mediated inhibition in Plasmodium falciparum.顶端膜抗原-1中的等位基因多态性导致恶性疟原虫逃避抗体介导的抑制作用。
Mol Microbiol. 2004 Apr;52(1):159-68. doi: 10.1111/j.1365-2958.2003.03974.x.

单微管:通过菱形蛋白酶-1定位鉴定出的恶性疟原虫裂殖子中的一种新分泌细胞器。

Mononeme: a new secretory organelle in Plasmodium falciparum merozoites identified by localization of rhomboid-1 protease.

作者信息

Singh Subhash, Plassmeyer Matthew, Gaur Deepak, Miller Louis H

机构信息

Malaria Cell Biology Section, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 12735 Twinbrook Parkway, Rockville, MD 20852, USA.

出版信息

Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):20043-8. doi: 10.1073/pnas.0709999104. Epub 2007 Nov 28.

DOI:10.1073/pnas.0709999104
PMID:18048320
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2148419/
Abstract

Compartmentalization of proteins into subcellular organelles in eukaryotic cells is a fundamental mechanism of regulating complex cellular functions. Many proteins of Plasmodium falciparum merozoites involved in invasion are compartmentalized into apical organelles. We have identified a new merozoite organelle that contains P. falciparum rhomboid-1 (PfROM1), a protease that cleaves the transmembrane regions of proteins involved in invasion. By immunoconfocal microscopy, PfROM1 was localized to a single, thread-like structure on one side of the merozoites that appears to be in close proximity to the subpellicular microtubules. PfROM1 was not found associated with micronemes, rhoptries, or dense granules, the three identified secretory organelles of invasion. Release of merozoites from schizonts resulted in the movement of PfROM1 from the lateral asymmetric localization to the merozoite apical pole and the posterior pole. We have named this single thread-like organelle in merozoites, the mononeme.

摘要

真核细胞中蛋白质在亚细胞细胞器内的区室化是调节复杂细胞功能的一种基本机制。恶性疟原虫裂殖子中许多参与入侵的蛋白质被区室化到顶端细胞器中。我们鉴定出了一种新的裂殖子细胞器,它含有恶性疟原虫菱形蛋白酶-1(PfROM1),一种能切割参与入侵的蛋白质跨膜区的蛋白酶。通过免疫共聚焦显微镜观察,PfROM1定位于裂殖子一侧的单个丝状结构上,该结构似乎紧邻表膜下微管。未发现PfROM1与微小膜泡、棒状体或致密颗粒相关,这三种是已确定的参与入侵的分泌细胞器。裂殖子从裂殖体中释放导致PfROM1从侧向不对称定位移动到裂殖子顶端极和后端极。我们将裂殖子中的这种单丝状细胞器命名为单膜体。