FK506结合蛋白12.6调节小鼠嗜铬细胞分泌(英文)  

FKBP12.6 Regulates The Secretion of Adrenal Chromaffin Cell in Mice

作　　者：袁琦[1,2] 郭宁[3] 顾磊[1] 王珺[1] 王黎[3] 周专[3] 姬广聚[1] 

机构地区：[1]中国科学院生物物理研究所生物大分子国家重点实验室,北京100101 [2]中国科学院大学,北京100049 [3]北京大学分子医学研究所,北京100871

出　　处：《生物化学与生物物理进展》2014年第5期449-455,共7页Progress In Biochemistry and Biophysics

基　　金：supported by grants from National Basic Research Program of China(2011CB809104);The National Natural Science Foundation of China(31271228)~~

摘　　要：FK506结合蛋白12.6(FKBP12.6)能够结合并调控钙离子释放通道兰尼碱受体2型(RyR2)的开放,可能是儿茶酚胺分泌的重要调控器.利用FKBP12.6敲除小鼠模型,我们研究了FKBP12.6在肾上腺嗜铬细胞胞吐中的作用.结果表明,FKBP12.6在小鼠肾上腺嗜铬细胞中表达,而敲除FKBP12.6小鼠的嗜铬细胞中有正常的去极化引起的钙电流和胞吐作用.然而,FKBP12.6敲除会导致嗜铬细胞中出现增强的咖啡因引起的细胞整体钙瞬变和咖啡因引起的胞吐作用.结果提示,FKBP12.6调控肾上腺嗜铬细胞儿茶酚胺的分泌,这种调控作用是通过调节钙离子的释放而实现的.FKBP12.6是嗜铬细胞分泌的重要蛋白.FK506 binding protein 12.6 （FKBP12.6）, a protein that binds to and regulates the ryanodine receptor type 2 （RyR2） Ca2＋ release channels, may act as an important regulator of eatecholamine secretion. In the present study, the role of FKBP12.6 in the control of chromaffin cell exoeytosis has been investigated using FKBP12.6-null mice. The results showed that FKBP12.6 was expressed in mouse chromaffin cells; deletion of FKBP12.6 did not change the depolarization induced Ca2＋ current and exocytosis. However, deletion of FKBP12.6 resulted in an enhanced caffeine-induced global Ca2. transient and larger caffeine-induced exocytosis in chromatTln cells of mice. These results indicate that FKBP12.6 is involved in catecholamine secretion through regulation of Ca2＋ release channel in mouse chromaffin cells.

关 键 词：FKS06结合蛋白12 6 肾上腺素嗜铬细胞 儿茶酚胺 钙离子 胞吐作用 

分 类 号：Q6[生物学—生物物理学]