2014年第41卷第5期目录
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封面故事：战斗或逃跑反应是由机体内分泌的儿茶酚胺类激素(肾上腺素和去甲肾上腺素)所引发的，以使身体能够和敌人战斗或者逃离危险而得到生存．肾上腺嗜铬细胞的生理学功能是释放肾上腺素和去甲肾上腺素到血液中，使交感神经系统兴奋以应对外界的压力．这个激素的释放是一个受钙离子调控的精细过程．然而，对嗜铬细胞中细胞内钙释放和细胞分泌的关系仍然了解很少．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．姬广聚研究组利用FKBP12.6敲除小鼠模型，研究了FKBP12.6在肾上腺嗜铬细胞胞吐中的作用．发现FKBP12.6和RyR2共定位于靠近细胞膜附近的内质网上．共聚焦钙成像和细胞分泌检测表明敲除FKBP12.6蛋白会导致咖啡因引起的钙释放增加和细胞分泌增多．这些结果提示FKBP12.6调控了肾上腺嗜铬细胞的分泌．
(袁 琦，郭 宁，顾 磊，王 珺，王 黎，周 专，姬广聚. FK506结合蛋白12.6调节小鼠嗜铬细胞分泌，本期第449～455页)
Cover Story：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 catecholamine secretion. In the present study, the role of FKBP12.6 in the control of chromaffin cell exocytosis 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 chromaffin cells of mice. These results indicate that FKBP12.6 is involved in catecholamine secretion through regulation of Ca2+ release channel in mouse chromaffin cells.
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综述与专论
研究快报
研究报告
技术与方法
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