Src-family tyrosine kinases and the Ca2+ signal
Src-family tyrosine kinases and the Ca2+ signal
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DOI：
10.1016/j.bbamcr.2016.10.022
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发表时间：
2017-06-01
影响因子：
5.1
通讯作者：
Villalobo, Antonio
中科院分区：
文献类型：
--
作者：
Anguita, Estefania;Villalobo, Antonio
在这篇综述中，我们将描述非受体Src家族激酶(SFK)与由各种细胞外和细胞内刺激产生的钙瞬间失活细胞之间的丰富的串扰，从而导致不同的信号事件。SFK和钙离子之间的信息交换是相互的，因为它是双向流动的。这些激酶是导致钙信号产生的主要因素，反过来，钙信号调节SFK的活性和功能。我们将介绍SFKs如何在激活一系列受体后参与胞内钙升高的产生，以及清除这一钙信号的机制。我们将详细讨论SFK对参与这些事件的钙离子转运通道的调节作用。最后，还将概述钙离子感受器蛋白钙调蛋白在c-Src活性中的作用，以及对其他SFK的潜在作用。本文是由Claus Heizmann、Joachim Krebs和Jacques Haiech编辑的题为：ECS会议的特刊的一部分。(C)2016爱思唯尔B.V.保留所有权利。
In this review, we shall describe the rich crosstalk between non-receptor Src-family kinases (SFKs) and the Ca2+ transient generated inactivated cells by a variety of extracellular and intracellular stimuli, resulting in diverse signaling events. The exchange of information between SFKs and Ca2+ is reciprocal, as it flows in both directions. These kinases are main actors in pathways leading to the generation of the Ca2+ signal, and reciprocally, the Ca2+ signal modulates SFKs activity and functions. We will cover how SFKs participate in the generation of the cytosolic Ca2+ rise upon activation of a series of receptors and the mechanism of clearance of this Ca2+ signal. The role of SFKs modulating Ca2+-translocating channels participating in these events will be amply discussed. Finally, the role of the Ca2+ sensor protein calmodulin on the activity of c-Src, and potentially on other SFKs, will be outlined as well. This article is part of a Special Issue entitled: ECS Meeting edited by Claus Heizmann, Joachim Krebs and Jacques Haiech. (C) 2016 Elsevier B.V. All rights reserved.