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中文摘要
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项目摘要 线粒体功能障碍是几乎所有老年性神经退行性疾病的主要后果, 可能是暴露于各种环境毒素的结果,即使是轻微水平。令人惊奇的是, 申请人的实验室已经发现,一种细胞类型中的线粒体应激可以传递到远端细胞, 没有经历线粒体应激的细胞类型。在线虫C. 在神经系统中驱动ETC复合物IV亚基的dsRNA表达的线虫中,它具有 已经表明,神经元线粒体应激可以传递到远端细胞,如肠。的 神经系统沟通这种轻微压力的能力会增加寿命和生存的时间。 整个动物。拟议研究的目标是确定这种信号的来源和性质 机制
英文摘要
Project Summary Mitochondrial dysfunction is a primary consequence of nearly all age-onset neurodegenerative diseases, and can be the consequence of exposure to even mild levels of a wide-range of environmental toxins. Surprisingly, the applicant's lab has uncovered that mitochondrial stress in one cell type can be communicated to a distal cell type that has not undergone mitochondrial stress. Using issue specific promoters in the nematode C. elegans that drive expression of dsRNA of a subunit of complex IV of the ETC in the nervous system, it has been shown that neuronal mitochondrial stress can be communicated to distal cells, such as the intestine. The ability of the nervous system to communicate this mild stress results in increased longevity and survival of the entire animal. The goal of the proposed studies is to identify the source and nature of this signaling mechanism.
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Extracellular Matrix Control of Mitochondrial Homeostasis and Longevity
  • 批准号:
    10722664
  • 项目类别:
  • 资助金额:
    $38.73万
  • 财政年份:
    2023
  • 负责人:
    Andrew G Dillin
  • 依托单位:
Glial regulation of longevity through a transcellular unfolded protein response
  • 批准号:
    10383697
  • 项目类别:
  • 资助金额:
    $39.25万
  • 财政年份:
    2018
  • 负责人:
    Andrew G Dillin
  • 依托单位:
Glial regulation of longevity through a transcellular unfolded protein response
The Collapse of Proteostasis during Aging is Mediated by Cytoskeletal Actin Functions
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