Synaptotagmin IV regulates dense core vesicle (DCV) release in LβT2 cells
Synaptotagmin IV regulates dense core vesicle (DCV) release in LβT2 cells
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DOI：
10.1016/j.bbrc.2008.04.174
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发表时间：
2008-07-11
影响因子：
3.1
通讯作者：
Wu, Zheng-Xing
中科院分区：
文献类型：
--
作者：
Hu, Zhi-Tao;Chen, Mao-Rong;Wu, Zheng-Xing
突触结合蛋白 (Syts) 是钙结合蛋白，从线虫到人类都是保守的。已在哺乳动物物种中鉴定出 15 种 Syt。 Syt I 被认为是某些类型神经元中突触小泡同步释放的 Ca2+ 传感器，但其在致密核心小泡 (DCV) 分泌中的作用仍不清楚。 Syt IV 的功能特别令人感兴趣，因为它会因慢性去极化和癫痫发作而迅速上调。利用 RNAi 介导的基因沉默，我们探索了 Syt I 和 IV 对垂体促性腺激素细胞系分泌的作用。 Syt IV 的下调明显减少了 L beta T2 细胞中 Ca2+ 触发的致密核心囊泡 (DCV) 的胞吐作用。然而，Syt I 沉默对囊泡释放没有影响。 (c) 2008 Elsevier Inc. 保留所有权利。
Synaptotagmins (Syts) are calcium-binding proteins which are conserved from nematodes to humans. Fifteen Syts have been identified in mammalian species. Syt I is recognized as a Ca2+ sensor for the synchFonized release of synaptic vesicles in some types of neurons, but its role in the secretion of dense core vesicles (DCVs) remains unclear. The function of Syt IV is of particular interest because it is rapidly up-regulated by chronic depolarization and seizures. Using RNAi-mediated gene silencing, we have explored the role of Syt I and IV on secretion in a pituitary gonadotrope cell line. Downregulation of Syt IV clearly reduced Ca2+-triggered exocytosis of dense core vesicles (DCVs) in L beta T2 cells. Syt I silencing, however, had no effect on vesicular release. (c) 2008 Elsevier Inc. All rights reserved.