Outward Trafficking of CFTR

CFTR 的向外贩运

• 批准号: 8134431
• 负责人: William B. Guggino
• 金额: $ 37.93万
• 依托单位: JOHNS HOPKINS UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-09-15 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/8134431
• 关键词: Abbreviations; Address; Adenoviruses; Affect; Apical; Area; Binding; Cell membrane; Cell surface; Cells; Complex; Critical Pathways; Cystic Fibrosis; Cystic Fibrosis Transmembrane Conductance Regulator; Data; Endoplasmic Reticulum Degradation Pathway; Epithelial; Epithelial Cells; Epithelium; GTPase TC10; GTPase-Activating Proteins; Goals; Golgi Apparatus; Grant; Hair; Human; Ligands; Macromolecular Complexes; Membrane; Molecular Weight; PDZ protein; Performance; Physiological; Physiological Processes; Plasma; Play; Process; Protein Binding; Proteins; Protons; Quality Control; RNA Interference; Regulation; Research Personnel; Role; SNAP receptor; Site; Sodium; Surface; Tight Junctions; Tissues; Ubiquitination; cold temperature; drug development; ezrin; insight; knock-down; member; moesin; new technology; novel; programs; protein folding; radixin protein; research study; syntaxin 6; trafficking; trans-Golgi Network

The experiments described within this proposal represent a new area of Invesfigation with implicafions for our understanding of A508-CFTR processing and trafficking. Identification ofthe critical pathways and establishment of their roles will pave the way forthe development of drugs to therapeutically alter the switching mechanisms that determine A508-CFTR's fate in Cystic Fibrosis. PROJECT/PERFORIVIANCE SITE(S) (if additional space is needed, use Project/Perfonnance Site Fonnat Page) Project/Performance

该建议中描述的实验代表了一个新的研究领域， 我们对A508-CFTR处理和贩运的了解。确定关键途径， 确立它们的作用将为药物的开发铺平道路， 决定A508-CFTR在囊性纤维化中命运的开关机制。 项目/执行地点（如果需要额外空间，请使用项目/执行地点格式页） 项目/业绩