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靶向疟原虫裂殖子表面蛋白1(MSP-1)的小分子可阻止宿主受到不同疟原虫物种的侵袭。

Small molecule targeting malaria merozoite surface protein-1 (MSP-1) prevents host invasion of divergent plasmodial species.

作者信息

Chandramohanadas Rajesh, Russell Bruce, Liew Kingsley, Yau Yin Hoe, Chong Alvin, Liu Min, Gunalan Karthigayan, Raman Rahul, Renia Laurent, Nosten Francois, Shochat Susana Geifman, Dao Ming, Sasisekharan Ram, Suresh Subra, Preiser Peter

机构信息

Interdisciplinary Research Group of Infectious Diseases, Singapore MIT Alliance for Research and Technology Centre (SMART) Singapore University of Technology and Design, 20 Dover Drive.

Interdisciplinary Research Group of Infectious Diseases, Singapore MIT Alliance for Research and Technology Centre (SMART).

出版信息

J Infect Dis. 2014 Nov 15;210(10):1616-26. doi: 10.1093/infdis/jiu296. Epub 2014 May 26.

Abstract

Malaria causes nearly 1 million deaths annually. Recent emergence of multidrug resistance highlights the need to develop novel therapeutic interventions against human malaria. Given the involvement of sugar binding plasmodial proteins in host invasion, we set out to identify such proteins as targets of small glycans. Combining multidisciplinary approaches, we report the discovery of a small molecule inhibitor, NIC, capable of inhibiting host invasion through interacting with a major invasion-related protein, merozoite surface protein-1 (MSP-1). This interaction was validated through computational, biochemical, and biophysical tools. Importantly, treatment with NIC prevented host invasion by Plasmodium falciparum and Plasmodium vivax--major causative organisms of human malaria. MSP-1, an indispensable antigen critical for invasion and suitably localized in abundance on the merozoite surface represents an ideal target for antimalarial development. The ability to target merozoite invasion proteins with specific small inhibitors opens up a new avenue to target this important pathogen.

摘要

疟疾每年导致近100万人死亡。最近多药耐药性的出现凸显了开发针对人类疟疾的新型治疗干预措施的必要性。鉴于糖结合疟原虫蛋白参与宿主入侵,我们着手将此类蛋白鉴定为小聚糖的靶点。结合多学科方法,我们报告发现了一种小分子抑制剂NIC,它能够通过与一种主要的入侵相关蛋白——裂殖子表面蛋白1(MSP-1)相互作用来抑制宿主入侵。这种相互作用通过计算、生化和生物物理工具得到了验证。重要的是,用NIC进行治疗可防止恶性疟原虫和间日疟原虫(人类疟疾的主要致病生物)的宿主入侵。MSP-1是一种对入侵必不可少的抗原,在裂殖子表面大量且适当地定位,是抗疟疾药物开发的理想靶点。用特定的小抑制剂靶向裂殖子入侵蛋白的能力为针对这种重要病原体开辟了一条新途径。

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