Modelling mechanisms of membrane shaping, fusion, and fission in endo- and exocytosis by protein scaffolds (A26*)

通过蛋白质支架模拟胞吞和胞吐作用中的膜成形、融合和裂变机制 (A26*)

• 批准号: 425958185
• 金额: --
• 依托单位: Department of Physiology and Pharmacology
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2019
• 资助国家: 德国
• 起止时间: 2018-12-31 至 2022-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/425958185?language=en
• 关键词: Modelling; mechanisms; membrane; shaping; fusion

We will use the theory of membrane elasticity to address key mechanisms of membrane remodelling in: clathrin-mediated endocytosis mediated by BAR family proteins in conjunction with dynamin and clathrin adaptors; clathrin independent endocytosis at synapses mediated by actin-myosin complexes; and synaptic vesicle exocytosis in the presynaptic active zone mediated by scaffolding proteins. The goal is to provide testable predictions for the experimental projects (A01), (A07), (A12), (Z02), (A03), (A05), and (A06) and complement the results of numerical simulations performed by (A04).

我们将使用膜弹性理论来解决膜重塑的关键机制：网格蛋白介导的内吞作用是由Bar家族蛋白与Dynamin和Clathrin适配器一起介导的；肌动蛋白膜蛋白复合物介导的突触中网格蛋白独立的内吞作用；以及由脚手架蛋白介导的突触前活性区域的突触囊泡胞吐作用。目的是为实验项目（A01），（A07），（A12），（Z02），（A03），（A03），（A05）和（A06）提供可测试的预测，并补充（A04 ）。