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心肌细胞及表达克隆受体基因的细胞中毒蕈碱型乙酰胆碱受体功能的调节

Regulation of muscarinic acetylcholine receptor function in cardiac cells and in cells expressing cloned receptor genes.

作者信息

Shapiro R A, Tietje K M, Subers E M, Scherer N M, Habecker B A, Nathanson N M

出版信息

Trends Pharmacol Sci. 1989 Dec;Suppl:43-6.

PMID:2694522
Abstract

The regulation of the number and function of the muscarinic receptors has been investigated in cultured chick cardiac cells and in cells expressing cloned genes encoding mammalian, Drosophila, and chick muscarinic receptors. A serum-free defined medium for the culture of chick embryonic heart cells has been used to study the regulation of mAChR number and function by serum lipoproteins. Addition of rooster high density lipoprotein to the culture medium results in an attenuation of muscarinic receptor-mediated inhibition of cAMP accumulation without a change in the number of receptors or inhibitory G proteins. Clones encoding the mouse m1 receptor and a homologous receptor from Drosophila have been isolated. When expressed in Y1 adrenal cells, both receptors stimulate phosphoinositide hydrolysis but do not inhibit cAMP accumulation. Deletion of 123 out of the 156 amino acids in the third cytoplasmic loop of the mouse m1 receptor does not impair its ability to stimulate phosphoinositide hydrolysis. A genomic clone encoding a muscarinic receptor expressed in chick heart has been isolated. When expressed in Y1 cells, it causes inhibition of cAMP accumulation but does not stimulate phosphoinositide hydrolysis.

摘要

已在培养的鸡心脏细胞以及表达编码哺乳动物、果蝇和鸡毒蕈碱受体的克隆基因的细胞中研究了毒蕈碱受体数量和功能的调节。一种用于培养鸡胚心脏细胞的无血清限定培养基已被用于研究血清脂蛋白对毒蕈碱型乙酰胆碱受体(mAChR)数量和功能的调节。向培养基中添加公鸡高密度脂蛋白会导致毒蕈碱受体介导的cAMP积累抑制作用减弱,而受体数量或抑制性G蛋白数量没有变化。已分离出编码小鼠m1受体和果蝇同源受体的克隆。当在Y1肾上腺细胞中表达时,两种受体均刺激磷酸肌醇水解,但不抑制cAMP积累。小鼠m1受体第三个细胞质环中156个氨基酸中的123个缺失并不损害其刺激磷酸肌醇水解的能力。已分离出一个在鸡心脏中表达的毒蕈碱受体的基因组克隆。当在Y1细胞中表达时,它会导致cAMP积累的抑制,但不刺激磷酸肌醇水解。

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1
Regulation of muscarinic acetylcholine receptor function in cardiac cells and in cells expressing cloned receptor genes.心肌细胞及表达克隆受体基因的细胞中毒蕈碱型乙酰胆碱受体功能的调节
Trends Pharmacol Sci. 1989 Dec;Suppl:43-6.
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