Poburko Damon, Kuo Kuo-Hsing, Dai Jiazhen, Lee Cheng-Han, van Breemen Cornelis
The Department of Pharmacology & Therapeutics, The University of British Columbia, Vancouver, British Columbia V6T 1Z1, Canada.
Trends Pharmacol Sci. 2004 Jan;25(1):8-15. doi: 10.1016/j.tips.2003.10.011.
Numerous cellular processes are regulated by fluctuations in the concentration of a single cation, Ca(2+). To accomplish this feat, cells have developed mechanisms that target Ca(2+) signals to specific effectors in both space, by strategically localizing effectors and ion-transporting molecules, and time, by encoding the regulation of the frequency of Ca(2+) oscillations. With an emphasis on smooth muscle, we have analyzed how the interaction of Ca(2+) transporters located on closely apposing membranes of the plasma membrane, sarcoplasmic reticulum and mitochondria provides the structural foundation for site-specific and time-specific Ca(2+) signaling. These junctional membrane complexes can either control the concentration of Ca(2+) in the microdomain that surrounds an effector molecule or deliver Ca(2+) from the translocator on one membrane to a second translocator on the opposing membrane without significant diffusion into the bulk cytosol, an event we term 'linked Ca(2+) transport'.
众多细胞过程受单一阳离子Ca(2+)浓度波动的调节。为实现这一功能,细胞已发展出多种机制,这些机制通过策略性地定位效应器和离子转运分子,在空间上使Ca(2+)信号靶向特定效应器;通过编码对Ca(2+)振荡频率的调节,在时间上实现这一目标。以平滑肌为重点,我们分析了位于质膜、肌浆网和线粒体紧密相邻膜上的Ca(2+)转运体之间的相互作用如何为位点特异性和时间特异性Ca(2+)信号传导提供结构基础。这些连接膜复合物既可以控制围绕效应分子的微区内Ca(2+)的浓度,也可以将Ca(2+)从一个膜上的转运体传递到相对膜上的另一个转运体,而不会大量扩散到细胞质中,我们将这一事件称为“连锁Ca(2+)转运”。