Transcriptional Regulation in Plasmodium falciparum

恶性疟原虫的转录调控

• 批准号: 6511631
• 负责人: KEVIN MILITELLO
• 金额: $ 3.83万
• 依托单位: HARVARD SCHOOL OF PUBLIC HEALTH
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-07-01 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/6511631
• 关键词: Plasmodium falciparum; affinity chromatography; gel mobility shift assay; gene expression; genetic promoter element; genetic regulatory element; genetic transcription; heat shock proteins; malaria; mass spectrometry; molecular pathology; nuclear runoff assay; regulatory gene; transcription factor

DESCRIPTION (provided by the applicant): Human malaria results from infection by the protozoan parasite Plasmodium sp. Currently, 300-500 million peoples are infected with malaria, and 1.5-3.5 million individuals succumb annually to the disease. Although expression of many P. falciparum genes involved in pathogenesis and development are regulated at the level of transcription, there is little mechanistic information regarding transcription in these organisms. Thus, transcription of three P. falciparum heat shock genes will be analyzed as a model system. Nuclear run on assays will be used to determine the transcription rates of these genes in the absence and presence of heat stress. In vivo reporter assays will be used to determine the promoter sequences required for transcription. Proteins that require transcription of the heat shock genes will be purified by DNA affinity chromatography and identified by mass spectroscopy. These studies will enhance our understanding of transcription in P. falciparum, and allow a better understanding of pathogenesis, differentiation, and drug resistance in this parasite.

描述（申请人提供）：人类疟疾是由感染引起的 由原生动物寄生虫Sp。目前，300-50万人是 感染疟疾，每年15-350万人屈服于 疾病。尽管许多参与的恶性疟原虫基因的表达 发病机理和发育受到转录水平的调节， 是关于这些生物中转录的几乎没有机械信息。 因此，将分析三个恶性疟原虫热休克基因的转录为 模型系统。测定法的核跑步将用于确定 这些基因在不存在和存在热应激的情况下的转录速率。 体内报告基因测定将用于确定启动子序列 转录所需的。需要热量转录的蛋白质 电击基因将通过DNA亲和色谱纯化，并通过 质谱。这些研究将增强我们对 在恶性疟原虫中的转录，可以更好地理解 该寄生虫的发病机理，分化和耐药性。