Decuypere Jean-Paul, Monaco Giovanni, Bultynck Geert, Missiaen Ludwig, De Smedt Humbert, Parys Jan B
Laboratory of Molecular and Cellular Signalling, Dept. Molecular and Cellular, campus Gasthuisberg O/N1 K.U.Leuven, Bus 802, B-3000 Leuven, Belgium.
Biochim Biophys Acta. 2011 May;1813(5):1003-13. doi: 10.1016/j.bbamcr.2010.11.023. Epub 2010 Dec 10.
The amount of Ca(2+) taken up in the mitochondrial matrix is a crucial determinant of cell fate; it plays a decisive role in the choice of the cell between life and death. The Ca(2+) ions mainly originate from the inositol 1,4,5-trisphosphate (IP(3))-sensitive Ca(2+) stores of the endoplasmic reticulum (ER). The uptake of these Ca(2+) ions in the mitochondria depends on the functional properties and the subcellular localization of the IP(3) receptor (IP(3)R) in discrete domains near the mitochondria. To allow for an efficient transfer of the Ca(2+) ions from the ER to the mitochondria, structural interactions between IP(3)Rs and mitochondria are needed. This review will focus on the key proteins involved in these interactions, how they are regulated, and what are their physiological roles in apoptosis, necrosis and autophagy. This article is part of a Special Issue entitled: 11th European Symposium on Calcium.
线粒体基质中摄取的Ca(2+)量是细胞命运的关键决定因素；它在细胞生死抉择中起决定性作用。Ca(2+)离子主要来源于内质网（ER）中对肌醇1,4,5-三磷酸（IP(3)）敏感的Ca(2+)储存库。线粒体对这些Ca(2+)离子的摄取取决于IP(3)受体（IP(3)R）在线粒体附近离散区域的功能特性和亚细胞定位。为了使Ca(2+)离子从内质网高效转移到线粒体，IP(3)R与线粒体之间需要结构相互作用。本综述将聚焦于参与这些相互作用的关键蛋白、它们如何被调控以及它们在凋亡、坏死和自噬中的生理作用。本文是名为：第11届欧洲钙研讨会的特刊的一部分。
