ASPARAGINE-LINKED OLIGOSACCHARIDE BIOSYNTHESIS

天冬酰胺连接低聚糖生物合成

• 批准号: 3447264
• 负责人: ANN E CHAPMAN
• 金额: $ 5.32万
• 依托单位: UT SOUTHWESTERN MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 1984
• 资助国家: 美国
• 起止时间: 1984-04-01 至 1987-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3447264
• 关键词: asparagine; carbohydrate biosynthesis; cell membrane; cell type; glucose metabolism; insulin; liver metabolism; membrane activity; muscle metabolism; oligosaccharides; ovary; sarcoplasmic reticulum; tissue /cell culture

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.

中文天冬酰胺连接寡糖合成的前期研究 仓鼠卵巢细胞已证明葡萄糖饥饿会导致 由于异常导致天冬酰胺连接的寡糖合成异常 脂质连接寡糖合成。 该提案的目的是 进一步研究脂质连接缺陷的性质 这些细胞中寡糖的合成，此外，还研究了 糖蛋白加工在以下条件下改变的可能性 葡萄糖饥饿或葡萄糖过量。 待研究的第二个系统的天冬酰胺连接的改变 低聚糖合成是BB/W糖尿病大鼠。 糖尿病，这是 其特点是缺乏胰岛素，导致无法 一些组织吸收葡萄糖，并且组织吸收过量的葡萄糖 葡萄糖摄取与胰岛素无关。 这些调查将集中于 肝脏和骨骼肌中糖基化的改变，以便 确定葡萄糖饥饿或过量葡萄糖是否会影响 天冬酰胺连接的寡糖体内合成的调节 生理条件。 由于异常的糖基化会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 关于天冬酰胺连接寡糖合成的关键调控点， 并且应该对未来糖蛋白合成改变的研究有用 或在糖尿病或其他血糖异常的系统中发挥作用 发生浓度。