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容量性钙内流。以胶质瘤C6细胞作为非兴奋性细胞模型。

Capacitative calcium entry. Glioma C6 as a model of nonexcitable cells.

作者信息

Barańska J, Przybyłek K, Sabała P

机构信息

Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology, Warszawa, Poland.

出版信息

Pol J Pharmacol. 1999 Mar-Apr;51(2):153-62.

PMID:10425644
Abstract

Although the mechanism of the capacitative Ca2+ entry is still a mysterious process, it has been presently accepted that it occurs through plasma membrane channel pores rather than through a carrier mechanism. As it has been proposed by Putney (Cell Calcium, 1986, 7, 1-12), Ca2+ entry is directly dependent on the state of filling of the endoplasmic reticulum Ca2+ stores, i.e. it is activated by the depletion of the endoplasmic reticulum Ca2+ pool. However, the nature of the signal for activation of Ca2+ entry is still unknown. The biphasic capacitative Ca2+ entry involves inositol phosphate system and is ubiquitous in all nonexcitable cells. We have shown that glioma C6 cells belong to such type of cells and are characterized by a typical capacitative Ca2+ entry pathway. The characteristics of this Ca2+ influx is summarized and the hypotheses about its mechanism of activation are discussed.

摘要

尽管容量性Ca2+内流的机制仍是一个神秘的过程,但目前已被接受的是,它通过质膜通道孔发生,而非通过载体机制。正如Putney(《细胞钙》,1986年,第7卷,第1 - 12页)所提出的,Ca2+内流直接依赖于内质网Ca2+储存的充盈状态,即它由内质网Ca2+池的耗竭所激活。然而,激活Ca2+内流的信号的本质仍然未知。双相容量性Ca2+内流涉及肌醇磷酸系统,且在所有非兴奋性细胞中普遍存在。我们已经表明,胶质瘤C6细胞属于此类细胞,并具有典型的容量性Ca2+内流途径。总结了这种Ca2+内流的特征,并讨论了关于其激活机制的假说。

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