Evidence for a vesicle-mediated maintenance of store-operated calcium channels in a human embryonic kidney cell line
Evidence for a vesicle-mediated maintenance of store-operated calcium channels in a human embryonic kidney cell line
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DOI：
10.1054/ceca.2000.0144
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发表时间：
2000-09-01
期刊：
影响因子：
4
通讯作者：
Steinhardt, RA
中科院分区：
文献类型：
--
作者：
Alderton, JM;Ahmed, SA;Steinhardt, RA
将梭菌神经毒素肉毒杆菌神经毒素一种轻链或破伤风神经毒素直接微量注射到人胚胎肾细胞系的细胞中，在体内钙储存被环吡唑酸耗尽后，显著减少钙的进入，环吡唑酸是肌浆-内质网状钙atp酶的可逆抑制剂。肉毒杆菌神经毒素A轻链特异性水解突触体相关蛋白25千顿（SNAP-25），破伤风神经毒素特异性水解突触蛋白-2（囊泡相关膜蛋白2，VAMP-2）和纤维素蛋白（囊泡相关膜蛋白3，VAMP-3）。由于这些底物蛋白是囊泡对接和融合所必需的，因此肉毒杆菌神经毒素、轻链和破伤风神经毒素对储存操作的钙进入的抑制支持了一种模型，即囊泡融合是激活储存操作的钙进入的先决条件。Brefeldin A是一种干扰囊泡交通的真菌代谢物，在钙储存耗尽后部分减少钙的进入。囊泡储备池的大小或平行囊泡循环途径使用brefeldin A敏感和brefeldin A不敏感的adp -核糖基化因子可以解释brefeldin A未能完全抑制储存操作的钙进入。(C) 2000 Harcourt出版社有限公司
Direct microinjection of the clostridial neurotoxins botulinum neurotoxin A light chain or tetanus neurotoxin into cells of a human embryonic kidney cell line significantly reduced calcium entry after depletion of internal calcium stores by cyclopiazonic acid, a reversible inhibitor of the sarcoplasmic-endoplasmic reticular calcium-ATPases. Botulinum neurotoxin A light chain specifically hydrolyzes a synaptosomal-associated protein of 25 kilodaltons (SNAP-25), and tetanus neurotoxin specifically hydrolyzes synaptobrevin-2 (vesicle-associated membrane protein 2, VAMP-2) and cellubrevin (vesicle-associated membrane protein 3, VAMP-3). Since these substrate proteins are required for vesicle docking and fusion, inhibition of store-operated calcium entry by botulinum neurotoxin A light chain and tetanus neurotoxin supports a model in which vesicle fusion is a prerequisite for activation of store-operated calcium entry. Brefeldin A, a fungal metabolite that interferes with vesicle traffic, partially reduced calcium entry following store depletion. The size of the reserve pool of vesicles or parallel vesicle recycling pathways employing brefeldin A-sensitive and brefeldin A-insensitive ADP-ribosylation factors may explain the failure of brefeldin A to completely inhibit store-operated calcium entry. (C) 2000 Harcourt Publishers Ltd.