Sarhan Adil R, Patel Trushar R, Creese Andrew J, Tomlinson Michael G, Hellberg Carina, Heath John K, Hotchin Neil A, Cunningham Debbie L
‡From the School of Biosciences, College of Life and Environmental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom.
‡From the School of Biosciences, College of Life and Environmental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom
Mol Cell Proteomics. 2016 Jun;15(6):1823-36. doi: 10.1074/mcp.M115.053652. Epub 2016 Apr 13.
Intracellular signaling pathways are reliant on protein phosphorylation events that are controlled by a balance of kinase and phosphatase activity. Although kinases have been extensively studied, the role of phosphatases in controlling specific cell signaling pathways has been less so. Leukocyte common antigen-related protein (LAR) is a member of the LAR subfamily of receptor-like protein tyrosine phosphatases (RPTPs). LAR is known to regulate the activity of a number of receptor tyrosine kinases, including platelet-derived growth factor receptor (PDGFR). To gain insight into the signaling pathways regulated by LAR, including those that are PDGF-dependent, we have carried out the first systematic analysis of LAR-regulated signal transduction using SILAC-based quantitative proteomic and phosphoproteomic techniques. We haveanalyzed differential phosphorylation between wild-type mouse embryo fibroblasts (MEFs) and MEFs in which the LAR cytoplasmic phosphatase domains had been deleted (LARΔP), and found a significant change in abundance of phosphorylation on 270 phosphosites from 205 proteins because of the absence of the phosphatase domains of LAR. Further investigation of specific LAR-dependent phosphorylation sites and enriched biological processes reveal that LAR phosphatase activity impacts on a variety of cellular processes, most notably regulation of the actin cytoskeleton. Analysis of putative upstream kinases that may play an intermediary role between LAR and the identified LAR-dependent phosphorylation events has revealed a role for LAR in regulating mTOR and JNK signaling.
细胞内信号通路依赖于由激酶和磷酸酶活性平衡所控制的蛋白质磷酸化事件。尽管激酶已得到广泛研究,但磷酸酶在控制特定细胞信号通路中的作用却较少被关注。白细胞共同抗原相关蛋白(LAR)是受体样蛋白酪氨酸磷酸酶(RPTPs)的LAR亚家族成员。已知LAR可调节多种受体酪氨酸激酶的活性,包括血小板衍生生长因子受体(PDGFR)。为深入了解由LAR调节的信号通路,包括那些依赖血小板衍生生长因子(PDGF)的信号通路,我们使用基于稳定同位素标记氨基酸的细胞培养(SILAC)的定量蛋白质组学和磷酸蛋白质组学技术,对LAR调节的信号转导进行了首次系统分析。我们分析了野生型小鼠胚胎成纤维细胞(MEF)与LAR胞质磷酸酶结构域已缺失的MEF(LARΔP)之间的磷酸化差异,发现由于LAR磷酸酶结构域的缺失,205种蛋白质上270个磷酸化位点的磷酸化丰度发生了显著变化。对特定的LAR依赖性磷酸化位点和富集的生物学过程的进一步研究表明,LAR磷酸酶活性影响多种细胞过程,最显著的是对肌动蛋白细胞骨架的调节。对可能在LAR与已确定的LAR依赖性磷酸化事件之间起中介作用的假定上游激酶的分析表明,LAR在调节哺乳动物雷帕霉素靶蛋白(mTOR)和应激活化蛋白激酶(JNK)信号传导中发挥作用。