ASPARAGINE-LINKED OLIGOSACCHARIDE BIOSYNTHESIS

中国人天冬酰胺连接低聚糖合成的研究进展 仓鼠卵巢细胞已经证明葡萄糖饥饿会导致 天冬酰胺连接低聚糖的异常合成 脂联寡糖的合成。这项提议的目的是 进一步探讨脂联素缺陷的本质 低聚糖在这些细胞中的合成，此外，研究 糖蛋白加工在以下条件下发生改变的可能性 葡萄糖缺乏或葡萄糖过多。 天冬酰胺连接的第二个系统将被研究改变 低聚糖的合成是BB/W糖尿病大鼠。糖尿病，这是 以胰岛素缺乏为特征的，这导致不能 一些组织摄取葡萄糖，以及组织对过量葡萄糖的摄取 胰岛素不依赖于葡萄糖摄取。这些调查将集中在 肝脏和骨骼肌的糖基化改变，以便 确定葡萄糖饥饿或过量葡萄糖是否会影响 天冬酰胺连接低聚糖在体内合成的调节 生理条件。 由于异常的糖基化可导致功能特性的改变 一些糖蛋白，这项研究的结果将提供信息 关于天冬酰胺连接的寡糖合成中的关键调节点， 这对未来糖蛋白合成的研究应该是有用的。 或在糖尿病或其他血糖异常的系统中起作用 就会发生集中。

Previous studies of asparagine-linked oligosaccharide synthesis in Chinese Hamster Ovary Cells have demonstrated that glucose-starvation leads to abnormal synthesis of asparagine-linked oligosaccharides due to abnormal lipid-linked oligosaccharide synthesis. It is the aim of this proposal to further investigate the nature in the defect in lipid-linked oligosaccharide synthesis in these cells and, in addition, investigate the possibility that glycoprotein processing is altered under conditions of glucose starvation or excess glucose. A second system to be investigated for alterations in asparagine-linked oligosaccharide synthesis is the BB/W diabetic rat. Diabetes, which is characterized by a deficiency of insulin, which leads to the inability of some tissues to take up glucose, and to excess glucose uptake by tissues insulin independent for glucose uptake. These investigations will focus on glycosylation alterations in liver and skeletal muscle, in order to determine whether glucose starvation or excess glucose can affect the regulation of asparagine-linked oligosaccharide synthesis in vivo under physiological conditions. Since abnormal glycolylation can lead to altered functional properties of some glycoproteins, the results of this study will provide information about key regulatory points in asparagine-linked oligosaccharide synthesis, and should be useful for future studies of altered glycoprotein synthesis or functions in diabetes or other systems where abnormal glucose concentrations occur.