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Investigating the role of Myosin VI in quality control of mitochondria linked to Parkinson's disease pathology

研究肌球蛋白 VI 在与帕金森病病理相关的线粒体质量控制中的作用

基本信息

批准号：
MR/N000048/1
负责人：
Folma Buss
金额：
$ 68.96万
依托单位：
University of Cambridge
依托单位国家：
英国
项目类别：
Research Grant
财政年份：
2016
资助国家：
英国
起止时间：
2016 至无数据
项目状态：
已结题

来源：
https://gtr.ukri.org/projects?ref=MR%2FN000048%2F1
关键词：
Investigating role Myosin VI quality

项目摘要

A significant proportion of our ageing population is affected by the late onset of neurodegenerative disorders such as Parkinson's, motor neuron or Alzheimer's disease. A better understanding of what causes these neurodegenerative diseases will lead to new therapeutic and preventive strategies. More and more research now suggests that Parkinson's disease and also other forms of dementia are caused by defects in a cellular pathway that is used to control the quality of mitochondria, our cellular power stations. If this turnover pathway and the replacement of 'old' mitochondria does not function properly, it can cause decreased energy production and the pile up of damaged mitochondria, which eventually in nerve cells causes them to die. Our research is focused on myosin VI, a molecular motor protein, which drives cargo along tracks to specific sites in the cell, rather like a train running along a railway network to its specific destinations. The cargo is hooked up to this motor with the help of specific adaptor proteins that we have previously identified in our research. New results show that this motor protein is recruited to damaged mitochondria and may play a role in their turn over and their quality control. We thus hope to identify the precise roles of myosin VI and its adaptor proteins in the pathway that is important for clearance of damaged mitochondria. This will open up new areas of research that may guide future clinical studies and the development of potential diagnostic tools and possible therapeutic strategies.

在本港老龄人口中，有相当比例的人患有迟发性神经退化疾病，例如帕金森氏症、运动神经元病或阿尔茨海默氏症。更好地了解是什么原因导致这些神经退行性疾病将导致新的治疗和预防策略。现在越来越多的研究表明，帕金森病和其他形式的痴呆症是由细胞通路中的缺陷引起的，该通路用于控制线粒体的质量，线粒体是我们的细胞发电站。如果这种周转途径和“旧”线粒体的替代不能正常工作，它可能会导致能量产生减少和受损线粒体的堆积，最终导致神经细胞死亡。我们的研究集中在肌球蛋白VI，一种分子运动蛋白，它驱动货物沿着轨道到达细胞中的特定部位，就像火车沿着沿着铁路网行驶到特定目的地一样。在我们先前研究中发现的特定衔接蛋白的帮助下，货物被连接到这个马达上。新的结果表明，这种运动蛋白被招募到受损的线粒体中，并可能在线粒体的翻转和质量控制中发挥作用。因此，我们希望确定肌球蛋白VI及其衔接蛋白在清除受损线粒体的重要途径中的确切作用。这将开辟新的研究领域，可能指导未来的临床研究和开发潜在的诊断工具和可能的治疗策略。