Coenzyme A synthesis in the human malaria parasite, Plasmodium falciparum

人类疟原虫恶性疟原虫中辅酶 A 的合成

• 批准号: nhmrc : 224245
• 负责人: A/Pr Kevin Saliba
• 金额: $ 28.56万
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2003
• 资助国家: 澳大利亚
• 起止时间: 2003-01-01 至 2005-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/coenzyme-synthesis-human-plasmodium-falciparum/95929
• 关键词: Coenzyme; synthesis; human; malaria; parasite

Malaria is responsible for hundreds of millions of cases and an estimated 1.5-2.7 million deaths each year. The disease is caused by a microscopic parasite which is becoming increasingly resistant to antimalarial drugs. There is a very real possibility that there will soon be parts of the world in which malaria is an untreatable disease, and there is an urgent need to identify new drug targets. This work focuses on a particular biochemical pathway in the human malaria parasite, Plasmodium falciparum. The pathway mediates the conversion of the nutrient, vitamin B5, into a molecule called Coenzyme A. It plays an essential role in the intraerythrocytic parasite and our preliminary data indicate that components of this pathway hold significant potential as antimalarial drug targets. In this project we will use a range of biochemical and molecular biology approaches to characterise in detail the components of this pathway in the parasite and to explore the possibility that compounds that inhibit this pathway may be of value as much-needed new antimalarial agents.

疟疾每年造成数亿病例，估计有 1.5-270 万人死亡。这种疾病是由一种微小寄生虫引起的，这种寄生虫对抗疟药物的抵抗力越来越强。很有可能很快世界上的某些地区疟疾将成为一种无法治愈的疾病，因此迫切需要确定新的药物靶点。这项工作重点关注人类疟原虫恶性疟原虫中的特定生化途径。该途径介导营养物质维生素 B5 转化为辅酶 A 分子。它在红细胞内寄生虫中发挥着重要作用，我们的初步数据表明该途径的成分具有作为抗疟药物靶点的巨大潜力。在这个项目中，我们将使用一系列生化和分子生物学方法来详细表征寄生虫中该途径的成分，并探索抑制该途径的化合物作为急需的新型抗疟药物的可能性。