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作 者:刘威[1] 段海清[1] 李淑琴[1] 刘秀丽[1] 张兆山[1]
机构地区:[1]军事医学科学院生物工程研究所,北京100071
出 处:《生物技术通讯》2004年第2期122-123,共2页Letters in Biotechnology
摘 要:μ型阿片受体是阿片类药物镇痛与成瘾的分子基础。从人脑组织总RNA通过RT-PCR法扩增获得μ型阿片受体的cDNA,将其克隆至pcDNA3.1穴+雪中,转染CHO细胞后筛选单克隆细胞株,检测重组细胞株表达的μ型阿片受体与激动剂慢性作用介导的胞内信号转导能力。通过激动剂慢性作用信号转导分析证实,DAMGO能够明显抑制吗啡慢性给药引起的重组细胞株胞内cAMP水平的上调作用,初步揭示了阿片受体与特异性配体相互作用的信号转导机制。opioid receptor is the molecular basis of analgesis and addiction of opioid drug. The cDNA of μ-type receptor was obtained by RT-PCR with whole RNA extracted from human brain, which was cloned into pcDNA3.1(+) followed by the positive plasmid were transfected into CHO cells with aid of liposome. After the monocloning cell being screened, the endocytic signal transduction ability of chronic treatment of agonist with μ-opioid receptor of recombinants was tested. The results indicate that DAMGO could inhibit obviously the superactivation of cAMP induced by morphine chronic treatment with recombinant, which would reveal preliminarily the signal transduction mechanism of interaction of opioid and specific ligand.
关 键 词:人 Μ型阿片受体 CAMP 信号转导机制 RT-PCR 上调作用
分 类 号:R338[医药卫生—人体生理学] Q78[医药卫生—基础医学]
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