ASPARAGINE-LINKED OLIGOSACCHARIDE BIOSYNTHESIS

中国人天冬酰胺连接寡糖合成的研究进展 卵巢细胞已经证明葡萄糖饥饿会导致 天冬酰胺连接寡糖的异常合成， 脂联寡糖合成。 本提案的目的是 进一步研究脂质连接缺陷的性质， 寡糖合成在这些细胞，此外，调查 糖蛋白加工在以下条件下改变的可能性： 葡萄糖饥饿或过量葡萄糖。 第二个系统将被研究用于天冬酰胺相关的改变 低聚糖合成是BB/W糖尿病大鼠。 糖尿病， 其特征在于胰岛素缺乏，这导致不能 一些组织吸收葡萄糖，组织过量吸收葡萄糖 胰岛素不依赖于葡萄糖摄取。 这些调查将集中在 肝脏和骨骼肌中的糖基化改变，以 确定葡萄糖饥饿或过量葡萄糖是否会影响 天冬酰胺连接的寡糖合成的调节 生理条件。 由于异常的糖基化可以导致改变的功能特性， 一些糖蛋白，这项研究的结果将提供信息 关于天冬酰胺连接寡糖合成的关键调控点， 这对今后糖蛋白合成改变的研究是有用的 或在糖尿病或其他系统中的功能， 浓度发生。

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.