通过可逆磷酸化和去磷酸化对肌醇1,4,5-三磷酸诱导的Ca2+释放的调节
Regulation of inositol 1,4,5-trisphosphate-induced Ca2+ release by reversible phosphorylation and dephosphorylation.
作者信息
Vanderheyden Veerle, Devogelaere Benoit, Missiaen Ludwig, De Smedt Humbert, Bultynck Geert, Parys Jan B
机构信息
Laboratory of Molecular and Cellular Signalling, Department Molecular and Cellular Biology, Campus Gasthuisberg O/N1-K. U. Leuven, Herestraat 49-Bus 802, B-3000 Leuven, Belgium.
出版信息
Biochim Biophys Acta. 2009 Jun;1793(6):959-70. doi: 10.1016/j.bbamcr.2008.12.003. Epub 2008 Dec 16.
Abstract
The inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) is a universal intracellular Ca2+-release channel. It is activated after cell stimulation and plays a crucial role in the initiation and propagation of the complex spatio-temporal Ca2+ signals that control cellular processes as different as fertilization, cell division, cell migration, differentiation, metabolism, muscle contraction, secretion, neuronal processing, and ultimately cell death. To achieve these various functions, often in a single cell, exquisite control of the Ca2+ release is needed. This review aims to highlight how protein kinases and protein phosphatases can interact with the IP3R or with associated proteins and so provide a large potential for fine tuning the Ca2+-release activity and for creating efficient Ca2+ signals in subcellular microdomains.
摘要
肌醇1,4,5-三磷酸（IP3）受体（IP3R）是一种普遍存在的细胞内Ca2+释放通道。它在细胞受到刺激后被激活，在复杂的时空Ca2+信号的起始和传播中起关键作用，这些信号控制着诸如受精、细胞分裂、细胞迁移、分化、代谢、肌肉收缩、分泌、神经处理以及最终细胞死亡等不同的细胞过程。为了实现这些通常在单个细胞中的各种功能，需要对Ca2+释放进行精确控制。本综述旨在强调蛋白激酶和蛋白磷酸酶如何与IP3R或相关蛋白相互作用，从而为微调Ca2+释放活性以及在亚细胞微域中产生有效的Ca2+信号提供巨大潜力。
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