Taylor Colin W, Tovey Stephen C, Rossi Ana M
Department of Pharmacology, University of Cambridge, Cambridge CB2 1PD, United Kingdom.
Cold Spring Harb Protoc. 2013 Oct 1;2013(10):914-7. doi: 10.1101/pdb.top066100.
Inositol 1,4,5-trisphosphate receptors (IP3Rs) are intracellular Ca(2+) channels. They are expressed in most animal cells and mediate release of Ca(2+) from the endoplasmic reticulum (ER) in response to the many stimuli that evoke formation of inositol 1,4,5-trisphosphate (IP3). The opening of individual IP3Rs causes small, transient, local increases in cytosolic Ca(2+) concentration, and these events are the fundamental units of Ca(2+) signaling. These openings allow Ca(2+) signals to be selectively delivered by individual channels to the specific Ca(2+) sensors that evoke cellular responses. Stimulation of IP3Rs by the Ca(2+) they release allows these tiny events to grow into much larger ones by recruitment of neighboring IP3Rs. Understanding how Ca(2+) effectively and specifically regulates so many cellular processes demands an understanding of the interplay between IP3 and Ca(2+) in controlling IP3R gating. Here, we briefly set the scene before introducing high-throughput methods that seek to address this issue.
肌醇1,4,5-三磷酸受体（IP3Rs）是细胞内的钙离子通道。它们在大多数动物细胞中表达，并响应多种刺激，介导内质网（ER）释放钙离子，这些刺激会引发肌醇1,4,5-三磷酸（IP3）的形成。单个IP3Rs的开放会导致胞质钙离子浓度出现小幅度、短暂的局部升高，这些事件是钙离子信号传导的基本单位。这些开放使得钙离子信号能够通过单个通道选择性地传递给引发细胞反应的特定钙离子传感器。IP3Rs释放的钙离子对其自身的刺激，会通过募集相邻的IP3Rs，使这些微小事件发展成更大的事件。要理解钙离子如何有效且特异性地调节如此众多的细胞过程，就需要了解IP3与钙离子在控制IP3R门控方面的相互作用。在此，我们在介绍旨在解决这一问题的高通量方法之前，先简要介绍一下背景情况。
