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本文引用的文献

1
Epitope mapping and topographic analysis of VAR2CSA DBL3X involved in P. falciparum placental sequestration.参与恶性疟原虫胎盘滞留的VAR2CSA DBL3X的表位作图与拓扑分析。
PLoS Pathog. 2006 Nov;2(11):e124. doi: 10.1371/journal.ppat.0020124.
2
Differential var gene transcription in Plasmodium falciparum isolates from patients with cerebral malaria compared to hyperparasitaemia.与高疟原虫血症患者相比,脑型疟患者恶性疟原虫分离株中var基因的差异转录。
Mol Biochem Parasitol. 2006 Dec;150(2):211-8. doi: 10.1016/j.molbiopara.2006.08.005. Epub 2006 Sep 5.
3
Differential expression of var gene groups is associated with morbidity caused by Plasmodium falciparum infection in Tanzanian children.var基因群组的差异表达与坦桑尼亚儿童因恶性疟原虫感染引起的发病率相关。
Infect Immun. 2006 Jul;74(7):3904-11. doi: 10.1128/IAI.02073-05.
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Virulence of malaria is associated with differential expression of Plasmodium falciparum var gene subgroups in a case-control study.在一项病例对照研究中,疟疾的毒力与恶性疟原虫var基因亚组的差异表达有关。
J Infect Dis. 2006 Jun 1;193(11):1567-74. doi: 10.1086/503776. Epub 2006 Apr 20.
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Structural basis for Duffy recognition by the malaria parasite Duffy-binding-like domain.疟原虫达菲结合样结构域识别达菲的结构基础。
Nature. 2006 Feb 9;439(7077):741-4. doi: 10.1038/nature04443. Epub 2005 Dec 21.
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Plasmodium falciparum variant surface antigen expression patterns during malaria.疟疾期间恶性疟原虫变异表面抗原的表达模式
PLoS Pathog. 2005 Nov;1(3):e26. doi: 10.1371/journal.ppat.0010026. Epub 2005 Nov 18.
7
Further definition of PfEMP-1 DBL-1alpha domains mediating rosetting adhesion of Plasmodium falciparum.介导恶性疟原虫玫瑰花结黏附的疟原虫红细胞膜蛋白-1(PfEMP-1)DBL-1α结构域的进一步定义。
Mol Biochem Parasitol. 2005 Nov;144(1):109-13. doi: 10.1016/j.molbiopara.2005.06.009.
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Structural basis for the EBA-175 erythrocyte invasion pathway of the malaria parasite Plasmodium falciparum.恶性疟原虫EBA-175红细胞入侵途径的结构基础
Cell. 2005 Jul 29;122(2):183-93. doi: 10.1016/j.cell.2005.05.033.
9
Artemisinin versus nonartemisinin combination therapy for uncomplicated malaria: randomized clinical trials from four sites in Uganda.青蒿素与非青蒿素联合疗法治疗单纯性疟疾:来自乌干达四个地点的随机临床试验
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10
Abnormal display of PfEMP-1 on erythrocytes carrying haemoglobin C may protect against malaria.携带血红蛋白C的红细胞上PfEMP-1的异常表达可能预防疟疾。
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恶性疟原虫疟疾严重疾病状态下的PfEMP1-DBL1α氨基酸基序

PfEMP1-DBL1alpha amino acid motifs in severe disease states of Plasmodium falciparum malaria.

作者信息

Normark Johan, Nilsson Daniel, Ribacke Ulf, Winter Gerhard, Moll Kirsten, Wheelock Craig E, Bayarugaba Justus, Kironde Fred, Egwang Thomas G, Chen Qijun, Andersson Björn, Wahlgren Mats

机构信息

Department of Microbiology and Tumor and Cell Biology (MTC), Karolinska Institutet and Swedish Institute for Infectious Diseases Control (SMI), Box 280, Nobels väg 16, SE-17177 Stockholm, Sweden.

出版信息

Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15835-40. doi: 10.1073/pnas.0610485104. Epub 2007 Sep 25.

DOI:10.1073/pnas.0610485104
PMID:17895392
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1994139/
Abstract

An infection with Plasmodium falciparum may lead to severe malaria as a result of excessive binding of infected erythrocytes in the microvasculature. Vascular adhesion is mediated by P. falciparum erythrocyte membrane protein-1 (PfEMP1), which is encoded for by highly polymorphic members of the var-gene family. Here, we profile var gene transcription in fresh P. falciparum trophozoites from Ugandan children with malaria through var-specific DBL1alpha-PCR amplification and sequencing. A method for subsectioning region alignments into homology areas (MOTIFF) was developed to examine collected sequences. Specific PfEMP1-DBL1alpha amino acid motifs correlated with rosetting and severe malaria, with motif location corresponding to distinct regions of receptor interaction. The method is potentially applicable to other families of variant proteins and may be useful in identifying sequence-phenotype relationships. The results suggest that certain PfEMP1 sequences are predisposed to inducing severe malaria.

摘要

恶性疟原虫感染可能会由于感染的红细胞在微血管中过度黏附而导致严重疟疾。血管黏附由恶性疟原虫红细胞膜蛋白1(PfEMP1)介导,该蛋白由var基因家族的高度多态性成员编码。在此,我们通过var特异性DBL1α-PCR扩增和测序,分析了来自乌干达患疟疾儿童的新鲜恶性疟原虫滋养体中的var基因转录情况。我们开发了一种将区域比对细分为同源区域(MOTIFF)的方法来检查收集到的序列。特定的PfEMP1-DBL1α氨基酸基序与红细胞凝聚和严重疟疾相关,基序位置对应于受体相互作用的不同区域。该方法可能适用于其他变体蛋白家族,并且可能有助于识别序列-表型关系。结果表明,某些PfEMP1序列易于诱发严重疟疾。