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.

先前关于中国天冬酰胺连接寡糖合成的研究 仓鼠卵巢细胞已经证明葡萄糖饥饿导致 由于异常而异常的白天连接寡糖的合成 脂质连接的寡糖合成。 这是该提议的目的 进一步研究脂质连接缺陷的性质 这些细胞中的寡糖合成，此外，还研究了 在 葡萄糖饥饿或多余的葡萄糖。 第二个要研究天冬酰胺连接改变的系统 寡糖合成是BB/W糖尿病大鼠。 糖尿病，就是 以胰岛素不足为特征，导致无法 一些组织吸收葡萄糖，并通过组织过多的葡萄糖吸收 胰岛素独立于葡萄糖摄取。 这些调查将重点 肝脏和骨骼肌的糖基化改变，以便 确定葡萄糖饥饿或多余的葡萄糖是否会影响 在体内调节天冬酰胺连接的寡糖合成 生理条件。 由于异常糖基化可能导致功能特性改变 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， 并且应该对改变糖蛋白合成的未来研究很有用 或功能在糖尿病或其他异常葡萄糖的系统中 发生浓度。