Protein Lipidation As a Regulator of Apoptotic Calcium Release: Relevance to Cancer.
Protein Lipidation As a Regulator of Apoptotic Calcium Release: Relevance to Cancer.
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DOI：
10.3389/fonc.2017.00138
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发表时间：
2017
影响因子：
4.7
通讯作者：
Boehning D
中科院分区：
文献类型：
--
作者：
Chen JJ;Boehning D
钙是细胞死亡途径的关键调节剂。导致细胞死亡的最接近的事件之一是质膜和内质网驻留钙通道的激活。大量证据表明，这一途径的缺陷有助于癌症的发展。虽然我们对细胞溶质和线粒体钙的下游升高如何导致细胞死亡有了深入的了解，但钙通道如何在凋亡刺激物的上游被激活还不太清楚。最近，它已被证明，蛋白质脂质化是一个有效的调节凋亡信号。尽管经典上认为是静态修饰，但快速且可逆的蛋白质酰化已成为与许多途径（包括钙释放和细胞死亡）相关的新信号传导范式。在这篇综述中，我们将讨论蛋白质脂质化在调节细胞凋亡钙信号中的作用，并与癌症的直接治疗相关。
Calcium is a critical regulator of cell death pathways. One of the most proximal events leading to cell death is activation of plasma membrane and endoplasmic reticulum-resident calcium channels. A large body of evidence indicates that defects in this pathway contribute to cancer development. Although we have a thorough understanding of how downstream elevations in cytosolic and mitochondrial calcium contribute to cell death, it is much less clear how calcium channels are activated upstream of the apoptotic stimulus. Recently, it has been shown that protein lipidation is a potent regulator of apoptotic signaling. Although classically thought of as a static modification, rapid and reversible protein acylation has emerged as a new signaling paradigm relevant to many pathways, including calcium release and cell death. In this review, we will discuss the role of protein lipidation in regulating apoptotic calcium signaling with direct therapeutic relevance to cancer.