Investigation of Ephrin-A reverse signalling in pancreatic islets (B11)

胰岛中 Ephrin-A 反向信号传导的研究 (B11)

• 批准号: 83741037
• 金额: --
• 依托单位: Institut für Stoffwechselphysiologie
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2008
• 资助国家: 德国
• 起止时间: 2007-12-31 至 2011-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/83741037?language=en
• 关键词: Investigation; Ephrin; reverse; signalling; pancreatic

Adhesion among beta cells leads to the formation of pancreatic islets in the course of inherent beta cell differentiation. This cell-cell adhesion adaptively increases when the glucose concentration rises, and it is essential for physiologic insulin secretion. We have recently shown that beta cells adhere and communicate with each other via ephrin-A1 and ephrin-A5 as well as various EphA receptors (Cell (2007) 129: 359-370). Here we would like to identify and characterize the components of this adaptive signaling pathway in pancreatic beta cells and study its role in type II diabetes mellitus.

β细胞之间的粘附导致在固有β细胞分化过程中胰岛的形成。当葡萄糖浓度升高时，这种细胞与细胞的粘附会适应性地增加，这对于生理性胰岛素分泌至关重要。我们最近表明，β细胞通过肝配蛋白-A1和肝配蛋白-A5以及各种EphA受体相互粘附和通讯(Cell (2007) 129: 359-370)。在这里，我们想要鉴定和表征胰腺 β 细胞中这种适应性信号通路的组成部分，并研究其在 II 型糖尿病中的作用。