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作 者:崔宗杰[1] CUI Zong Jie(Institute of Cell Biology,Beijign Normal University,100875.Beijing,China)
机构地区:[1]北京师范大学细胞生物学研究所,北京100875
出 处:《北京师范大学学报(自然科学版)》2020年第1期1-8,共8页Journal of Beijing Normal University(Natural Science)
基 金:国家自然科学基金资助项目(31670856,61971170)。
摘 要:光敏剂磺酸化铝络酞菁(SALPC)光动力作用所产生的单线态氧分子(1O2),永久性激活分离大鼠胰腺腺泡细胞内源性的和在HEK293细胞异源表达的胆囊收缩素1型受体(cholecystokinin type 1 receptor, CCK1R).基因编码的蛋白质光敏剂(genetically encoded protein photosensitiser, GEPP)毒杀红(KillerRed)、迷你单(miniSOG)在胰腺腺泡肿瘤细胞系AR4-2J质膜定位表达后,光动力永久激活AR4-2J细胞内源性CCK1R.细胞特异性KillerRed或miniSOG光动力作用,有望为阐述CCK1R的生理功能提供直接证据.潜在"嘎嘣脆"受体嵌合体的出现,将可实现对其他G蛋白偶联受体的在体原位远程调控.本文综述了实验室发现"嘎嘣脆"受体(可被1O2永久性激活的G蛋白偶联受体)的相关工作背景和已发表的主要研究结果,展望该领域发展前景,预测"嘎嘣脆"受体在疾病治疗中的可能应用.Singlet oxygen(1O2) generated in type II photodynamic action with photosensitiser sulphonated aluminium phthalocyanine(SALPC) permanently activates cholecystokinin type 1 receptor(CCK1 R) endogenously expressed in isolated rat pancreatic acini or expressed ectopically in HEK293 cells. The emergence of genetically encoded protein photosensitisers makes possible plasma membrane-localized photodynamic action. Plasma membrane-localized photodynamic action with KillerRed or miniSOG activates CCK1 R in rat pancreatic acinar tumor cell AR4-2 J. Future in vivo cell type-specific photodynamic action is likely to provide direct evidence for the role of CCK1 R in defined physiological functions. Engineered chimeric receptors will enable the evaluation of other G protein-coupled receptors. In this brief review the author describes the background against which GPCR-ABSO was discovered, summarizes the major findings that have been published, and provides some perpectives about future works and their possible applications in clinical medicine.
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