Post-translational modification of myofilament proteins in the regulation of skeletal muscle contraction.

肌丝蛋白的翻译后修饰在骨骼肌收缩调节中的作用。

• 批准号: 404915-2012
• 负责人: Simpson, Jeremy
• 金额: $ 2.11万
• 依托单位: University of Guelph
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2017
• 资助国家: 加拿大
• 起止时间: 2017-01-01 至 2018-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=630437
• 关键词: Post; translational; modification; myofilament; proteins

Muscle contraction is the result of the complex interactions of many proteins. It is, ultimately, the interplay between the contractile proteins, in a calcium dependent manner, which produces force at the expense of ATP hydrolysis. Protein alterations (e.g., phosphorylation) are common mechanisms regulating or 'fine tuning' critical cellular processes. Alterations in one or more of the myofilament proteins, the proteins directly responsible for contraction, have the potential to affect force production and/or contractile economy. Exercise-induced fatigue can be characterized by temporary reductions in the ability to produce force. The goal of my research is to identify changes in myofilament proteins that occur in response to fatigue. Each protein alteration could be an adaptive or compensatory response to fatigue. There are no studies examining the time-related effects of fatiguing exercise on alterations to myofilament proteins. The is the first step in determining the significance of each myofilament alteration and delineating the molecular pathways which were activated to cause each specific alteration. The proposed studies, therefore, will generate new information about how alterations in skeletal myofilament proteins contribute to muscle fatigue. These studies have the potential to provide new insights into unappreciated aspects of how myofilament proteins contribute to fatigue. With a clearer understanding of the basic mechanisms regulating skeletal myofilament function, we will be in a better position to understand the regulation of skeletal muscle function.

肌肉收缩是许多蛋白质复杂相互作用的结果。最终，是收缩性蛋白质之间以钙依赖性方式的相互作用以ATP水解为代价产生力。蛋白质改变（例如，磷酸化）是调节或“微调”关键细胞过程的常见机制。一种或多种肌丝蛋白（直接负责收缩的蛋白质）的改变有可能影响力的产生和/或收缩经济性。运动诱发的疲劳可以通过产生力的能力的暂时降低来表征。我的研究目标是确定肌丝蛋白在疲劳时发生的变化。每种蛋白质的改变都可能是对疲劳的适应性或补偿性反应。没有研究检查疲劳运动对肌丝蛋白改变的时间相关影响。这是确定每个肌丝改变的意义和描绘被激活以引起每个特定改变的分子途径的第一步。因此，拟议的研究将产生关于骨骼肌肌丝蛋白的改变如何导致肌肉疲劳的新信息。这些研究有可能为肌丝蛋白如何导致疲劳的未被重视的方面提供新的见解。随着对骨骼肌肌丝功能调节的基本机制的了解，我们将更好地理解骨骼肌功能的调节。