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Interaction Efficiency of Drugs towards the Novel Membranous Structure Maurer's cleft for Malarial Disease

机译:药物对疟原虫裂缝裂缝的互动效率

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India, being a developing country, incidence of malarial infection prevailas a major socio-economic problem, though the infection is both treatable and preventable. There are nine anopheline vectors to transmit three specific Plasmodial species, P. falciparum, P. vivax and P. malariae, where the parasite develops intracellularly within the altered host red blood cell. Recently, it has been identified that a membranous structure called Maurer's Cleft (MC) is formed by P. falciparum for protein sorting and export in order to remodel the erythrocyte. The five major proteins involve are Plasmodium falciparum erythrocyte membrane protein 1 (PfEMPl), the ring-exported proteins (REX) 1 and 2, repetitive interspersed family (RIFINS), a subtelomeric variable open reading frame (STE-VORS) and Plasmodium falciparum Maurer's clefts two transmembrane protein (PfMC-2TM). Among REX 1 is reported to persists throughout the life cycle of the parasite and also involve a novel PEXEL (a motif which possess recessed signal sequence for entering the erythrocyte) independent export pathway. Most importantly, the role of REX 1 in the maintenance of MC architecture, where the truncation of REX 1 gene in P. falciparum strain D10 results in distortion of MC morphology and decrease in the number of MC. Addition to those MC cisternae seems stacked or multilamellate. Hence, REX 1 could serve as an exclusive target to intervene the process in erythrocyte remodelling and is considered for the present study. The present study indicates the significant interaction showed by the antimalarial drugs with REX1.
机译:印度是一个发展中国家,疟疾感染的发病率为Prevailas是一个主要的社会经济问题,尽管感染既可治疗和预防。有九种同源载体传递三种特异性疟原虫种类,P. falciparum,P.Vivax和P.Malariae,寄生虫在改变的宿主红细胞内形成细胞内。最近,已经确定了一种据标明称为Maurer裂缝(MC)的膜结构由P. Falciparum用于蛋白质分选和出口,以改造红细胞。五种主要蛋白质涉及疟原虫红细胞膜蛋白1(Pfempl),环出口蛋白(REX)1和2,重复的散射家族(Rifins),一个子制变量开放阅读框(STE-VORS)和疟原虫疟原虫Maurer的FLFTS两种跨膜蛋白(PFMC-2Tm)。据报道,在寄生虫的整个生命周期中据报道雷克斯1中,并且还涉及新的Pexel(具有用于进入红细胞的凹陷信号序列的基序)独立的出口途径。最重要的是,REX 1在MC架构维持中的作用,其中P.Malciparum菌株D10中的REX 1基因的截短导致MC形态的变形并减少MC的数量。除了那些Mc Cisternae似乎堆叠或多菱形。因此,REX 1可以作为介入红细胞重塑过程中的独占目标,并考虑本研究。本研究表明,抗疟药与REX1的显着相互作用。

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