Signalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.
Department of Biology, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
Sci Rep. 2023 Oct 25;13(1):18237. doi: 10.1038/s41598-023-45148-6.
Norbin is an adaptor protein that binds numerous G protein-coupled receptors (GPCRs), is highly expressed in neurons, and is essential for a functioning nervous system in rodent models. Yet, beyond its control of neurite outgrowth and synaptic plasticity, few cellular roles of Norbin have been investigated to date. Furthermore, while Norbin is known to regulate the steady-state cell surface levels of several GPCRs, only in one case has the protein been shown to control the agonist-induced receptor internalisation which serves to attenuate GPCR signalling. Here, we generated a Norbin-deficient PC12 cell line which enabled us to study both the cellular functions of Norbin and its roles in GPCR trafficking and signalling. We show that Norbin limits cell size and spreading, and is required for the growth, viability and cell cycle progression of PC12 cells. We also found that Norbin regulates both the steady-state surface level and agonist-induced internalisation of the GPCR sphingosine-1-phosphate receptor 1 (S1PR1) in these cells, suggesting that its role in agonist-dependent GPCR trafficking is more widespread than previously appreciated. Finally, we show that Norbin limits the S1P-stimulated activation of Akt and p38 Mapk, and is required for the activation of Erk in PC12 cells. Together, our findings provide a better understanding of the cellular functions of Norbin and its control of GPCR trafficking.
诺宾是一种衔接蛋白,可与许多 G 蛋白偶联受体(GPCR)结合,在神经元中高度表达,对啮齿动物模型的正常神经系统功能至关重要。然而,除了控制神经突生长和突触可塑性之外,迄今为止,很少有研究调查过诺宾的其他细胞功能。此外,尽管已知诺宾可调节几种 GPCR 的稳定细胞表面水平,但仅在一种情况下已证明该蛋白可控制激动剂诱导的受体内化,这有助于减弱 GPCR 信号。在这里,我们生成了一种缺乏诺宾的 PC12 细胞系,使我们能够研究诺宾的细胞功能及其在 GPCR 运输和信号转导中的作用。我们发现诺宾限制了细胞大小和扩展,并且是 PC12 细胞生长、活力和细胞周期进程所必需的。我们还发现,诺宾调节这些细胞中 GPCR 鞘氨醇-1-磷酸受体 1(S1PR1)的稳定表面水平和激动剂诱导的内化,这表明其在激动剂依赖性 GPCR 运输中的作用比以前认为的更为广泛。最后,我们表明诺宾限制了 S1P 刺激的 Akt 和 p38 Mapk 的激活,并需要诺宾在 PC12 细胞中激活 Erk。总之,我们的发现提供了对诺宾的细胞功能及其对 GPCR 运输的控制的更好理解。