α-LTX and α-LTX^(N4C) induce [Ca^(2+)]i elevation through different mechanisms in pancreatic β cells
α-LTX and α-LTX^(N4C) induce [Ca^(2+)]i elevation through different mechanisms in pancreatic β cells作者机构：Institute of Biophysics and Biochemistry School of Life Science and Technology Huazhong University of Science and Technology Wuhan 430074 China National Laboratory of Biomacromolecules Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China
出 版 物：《Chinese Science Bulletin》 (CHINESE SCIENCE BULLETIN)
年 卷 期：2006年第51卷第2期
页 面：158-163页
核心收录：
学科分类：100405[医学-卫生毒理学] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 10[医学]
基 金：We thank Prof.Yuri Ushkaryov for supplying α-LTXN4C.This work was supported by the National Natural Science Foundation of China(Grant Nos.30270363&30130230) the National Basic Research Program of China(Grant Nos.G1999054000&2004CB720000)
主 题：胰腺β细胞 α-LTX α-LTX^N4C 神经毒素 蜘蛛毒液 钙离子 毒性机制
摘 要：α-latrotoxin (α-LTX), a neurotoxin from black-widow spider, causes vesicles release in pre- synapse of nerve terminal after binding to specific membrane receptors. α-LTXN4C is an effective tool binding to calcium independent receptor for latrotoxin (CIRL), which is used to elucidate the mechanism of receptor-mediated signal pathway. In our study on the pancreatic β cells, we found that α-LTX inserts into the plasma membrane and forms stable non-selective cation channels. The influx of ex- tracellular Ca2+ through the channels causes massive Ca2+-dependent exocytosis of insulin-containing vesicles, whereas, α-LTXN4C, binding with its receptor CIRL in extracellular divalent cation-dependent way, increases [Ca2+]i by mobilization of the intracellular calcium stores.
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