The Endoplasmic Reticulum-Plasma Membrane Junction: A Hub for Agonist Regulation of Ca2+ Entry.
The Endoplasmic Reticulum-Plasma Membrane Junction: A Hub for Agonist Regulation of Ca2+ Entry.
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DOI：
10.1101/cshperspect.a035253
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发表时间：
2019-09
影响因子：
7.2
通讯作者：
H. L. Ong;I. Ambudkar
中科院分区：
文献类型：
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作者：
H. L. Ong;I. Ambudkar
细胞表面受体的刺激诱导细胞质Ca2+ ([Ca2+]i)增加，通过效应蛋白检测和转导来调节细胞功能。细胞内Ca2+释放，通过内质网（ER）蛋白肌醇1,4,5-三磷酸受体（IP3R）和ryanodine受体（RyR）， Ca2+内流，通过储存操作的Ca2+进入（SOCE），有助于[Ca2+]i的增加，[Ca2+]i增加的幅度，频率和空间特征是由蛋白质区隔化成信号复合物如受体-信号复合物和SOCE复合物控制。这两种复合物都包括位于质膜（PM）和内质网中的蛋白质和脂质成分。受体信号通过磷脂酶C （PLC）介导的磷脂酰肌醇4,5-二磷酸（PIP2）的水解在PM中启动，并随着内质网中IP3R的激活而达到高潮。相反，SOCE在内质网中由Ca2+感应基质相互作用分子（STIM）蛋白启动，然后与PM通道Orai1和TRPC1相互作用以激活Ca2+进入。这篇综述将讨论ER-PM连接如何在SOCE激动剂调节中发挥核心作用。
Stimulation of cell-surface receptors induces cytosolic Ca2+ ([Ca2+]i) increases that are detected and transduced by effector proteins for regulation of cell function. Intracellular Ca2+ release, via endoplasmic reticulum (ER) proteins inositol 1,4,5-trisphosphate receptors (IP3R) and ryanodine receptors (RyR), and Ca2+ influx, via store-operated Ca2+ entry (SOCE), contribute to the increase in [Ca2+]i The amplitude, frequency, and spatial characteristics of the [Ca2+]i increases are controlled by the compartmentalization of proteins into signaling complexes such as receptor-signaling complexes and SOCE complexes. Both complexes include protein and lipid components, located in the plasma membrane (PM) and ER. Receptor signaling initiates in the PM via phospholipase C (PLC)-mediated hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2), and culminates with the activation of IP3R in the ER. Conversely, SOCE is initiated in the ER by Ca2+-sensing stromal interaction molecule (STIM) proteins, which then interact with PM channels Orai1 and TRPC1 to activate Ca2+ entry. This review will address how ER-PM junctions serve a central role in agonist regulation of SOCE.