Mechanisms maintaining mitochondrial copper homeostasis.

维持线粒体铜稳态的机制。

• 批准号: DP220102030
• 负责人: Prof Megan Maher
• 金额: $ 39.59万
• 依托单位: The University of Melbourne
• 依托单位国家: 澳大利亚
• 项目类别: Discovery Projects
• 财政年份: 2022
• 资助国家: 澳大利亚
• 起止时间: 2022-05-17 至 2025-05-16
• 项目状态: 未结题
• 来源: https://dataportal.arc.gov.au/RGS/Web/Grants/DP220102030
• 关键词: Mechanisms; maintaining; mitochondrial; copper; homeostasis.

This project aims to define the molecular mechanisms by which copper is trafficked and balanced within mitochondria. The project will employ an integrated biological, biochemical, biophysical and structural approach to examine the proteins which underpin the balance between the essentiality for copper and its toxicity, within this organelle. This project will deliver fundamental insights into how mitochondria contribute to and achieve cellular metal homeostasis, in addition to molecular explanations for how faults in this process result in mitochondrial defects. Major benefits include research training, strengthened international linkages and fundamental insights into mitochondrial biochemistry.

该项目旨在确定铜在线粒体内运输和平衡的分子机制。该项目将采用综合的生物学、生物化学、生物物理和结构方法来检查在这个细胞器内支撑铜的重要性和其毒性之间平衡的蛋白质。该项目将提供线粒体如何促进和实现细胞金属稳态的基本见解，以及该过程中的错误如何导致线粒体缺陷的分子解释。主要的好处包括研究培训，加强国际联系和线粒体生物化学的基本见解。