Nuclear force feedback as rheostat for actomyosin tension control

核力反馈作为肌动球蛋白张力控制的变阻器

• 批准号: MR/Y001125/1
• 负责人: Tobias Zech
• 金额: $ 74.82万
• 依托单位: University of Liverpool
• 依托单位国家: 英国
• 项目类别: Research Grant
• 财政年份: 2024
• 资助国家: 英国
• 起止时间: 2024 至 无数据
• 项目状态: 未结题
• 来源: https://gtr.ukri.org/projects?ref=MR%2FY001125%2F1
• 关键词: Nuclear; force; feedback; rheostat; actomyosin

Ageing manifests itself on multiple levels in the body. Many cell types, such as blood vessel and adjacent cells are subject to constant mechanical challenges due to blood flow and constriction. In cells, ageing and pre-mature ageing syndroms such as Progeria cause several changes that make them more prone to damage when they are put under strain. In this project we are going to investigate how cells regulate their responds to strain and why this does not work in aged cells. We have found that the cytoskeleton, the scaffold that keeps cells in shape and motile, is under more tension that experience symptoms of ageing. This leads to decreased ability to respond to varying outside forces that are applied onto the cells and often causes cell death. In this application we will investigate the cause of this reduced adaptability to force. This will help in understanding the changes that ageing causes in cells and potentially will give rise to new avenues of research into developing treatments for these symptoms.

衰老体现在身体的多个层面。许多细胞类型，例如血管和邻近细胞，由于血流和收缩而受到持续的机械挑战。在细胞中，衰老和早衰综合症（例如早衰症）会引起一些变化，使细胞在承受压力时更容易受到损害。在这个项目中，我们将研究细胞如何调节对压力的反应，以及为什么这在衰老细胞中不起作用。我们发现，细胞骨架（保持细胞形状和活力的支架）承受更大的张力，从而出现衰老症状。这导致细胞对施加到细胞上的不同外力的反应能力下降，并常常导致细胞死亡。在此应用中，我们将调查这种对力的适应性降低的原因。这将有助于了解衰老引起的细胞变化，并有可能为开发这些症状的治疗方法提供新的研究途径。