DEFECTIVE CAMP DEPENDENT PHOSPHORYLATION IN SYSTEMIC LUPUS ERYTHEMAMOSUS

系统性红斑狼疮中营依赖性磷酸化缺陷

• 批准号: 6282754
• 负责人: GARY M KAMMER
• 金额: $ 3.63万
• 依托单位: WAKE FOREST UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1997
• 资助国家: 美国
• 起止时间: 1997-12-01 至 1998-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6282754
• 关键词: T lymphocyte; biological signal transduction; clinical research; cyclic AMP; enzyme activity; enzyme deficiency; human subject; isozymes; pathologic process; phosphorylation; phosphotransferases; protein kinase A; systemic lupus erythematosus

The multiple fault T-lymphocyte effector functions in systemic lupus erythematosus may result from altered signal transduction with a defective biochemical pathway(s). Impaired CAMP-inducible, protein kinase A(PKA) dependent protein phosphorylation in intact T-lymphocytes from subjects with mild to severe SLE due to deficient activity of the Type 1 isozyme of PKA(PKA- 1) have been demonstrated. He seeks to define the biochemical, molecular and genetic mechanisms leading to diminished PKA-1 phosphotransferase activity.

系统性红斑狼疮患者T淋巴细胞效应器功能的多重缺陷 红斑症可能是由于有缺陷的信号转导改变引起的 生化途径(S)。CAMP诱导的蛋白激酶A(PKA)受损 受试者完整T淋巴细胞中依赖蛋白的磷酸化 由于1型红斑狼疮同工酶活性不足而导致的轻到重度系统性红斑狼疮 PKA(PKA-1)已被证实。他试图定义生物化学， 导致PKA-1表达降低的分子和遗传机制 磷酸转移酶活性。