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.

中文翻译：

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内质网-质膜连接：Ca2+ 进入激动剂调节的枢纽。

细胞表面受体的刺激诱导细胞溶质 Ca2+ ([Ca2+]i) 增加，这些增加被效应蛋白检测和转导以调节细胞功能。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) 和兰尼碱受体 (RyR)，以及 Ca2+ 流入，通过储存操作的 Ca2+ 进入 (SOCE)，有助于增加 [ Ca2+]i [Ca2+]i 增加的幅度、频率和空间特征受蛋白质划分为信号复合物（如受体信号复合物和 SOCE 复合物）的控制。两种复合物都包括位于质膜 (PM) 和 ER 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) 水解在 PM 中启动，并最终在 ER 中激活 IP3R。相反，在 ER 中 SOCE 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。本综述将探讨 ER-PM 连接如何在 SOCE 的激动剂调节中发挥核心作用。