Molecular mechanisms of ARF family GTPases

ARF家族GTP酶的分子机制

• 批准号: 9893466
• 负责人: Richard A Kahn
• 金额: $ 9.54万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2017
• 资助国家: 美国
• 起止时间: 2017-09-15 至 2022-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9893466
• 关键词: Arl proteins; Biochemical; Biological; Cell physiology; Cells; Cellular biology; Centrosome; Cilia; Cytoskeleton; Cytosol; Energy Metabolism; Family; Functional disorder; Guanosine Triphosphate Phosphohydrolases; Heart Diseases; Human; Intervention; Malignant Neoplasms; Membrane Protein Traffic; Mitochondria; Molecular; Nerve Degeneration; Phylogenetic Analysis; Regulation; Retinal Degeneration; Signal Transduction; Site; System; ciliopathy; cilium biogenesis; deafness; human disease; insight; member; novel

Project Summary/Abstract Members of the ARF family of regulatory GTPases function as nodes in cell signaling to coordinate essential cell processes; including membrane traffic, energy metabolism, ciliogenesis, and the cytoskeleton. I have studied first ARF and later ARF-like (ARL) proteins for over 30 years, using a combination of biochemical, cell and molecular biological, and phylogenetic approaches and propose to continue these studies with a focus on their actions at specific sites; including mitochondria, cytosol, cilia, and centrosomes. We will both study mechanisms by which one GTPase acts in multiple sites in the same cells, to explore the potential for cross-talk or higher level ordering of cell signaling, but also explore novel, single actions for atypical GTPases as a means of determining shared or unique mechanisms within the family. A better understanding of these systems will reveal novel insights into fundamental aspects of cell biology as well as providing potential targets for intervention to alter the course of human diseases; including but not limited to cancer, heart disease, neurodegeneration, ciliopathies, retinal degeneration, and deafness.

项目总结/文摘