Voisin L, Larose L, Meloche S
Centre de Recherche, Centre hospitalier de l'Université de Montréal and Department of Pharmacology, University of Montreal, Campus Hôtel-Dieu, 3850 St. Urbain, Montreal, Quebec, Canada H2W 1T8.
Biochem J. 1999 Jul 1;341 ( Pt 1)(Pt 1):217-23.
Nck is a small adaptor protein consisting exclusively of three SH3 domains and one SH2 domain. Nck is thought to have an important role in cell signalling by coupling receptor tyrosine kinases, via its SH2 domain, to downstream SH3-binding effectors. We report here that angiotensin II, working through the AT1 receptor subtype, stimulates the phosphorylation of Nck in rat aortic smooth muscle cells. Phosphopeptide mapping analysis revealed that Nck is phosphorylated on four peptides containing exclusively phosphoserine in quiescent cells. Treatment with angiotensin II resulted in increased phosphorylation of these four peptides, without the appearance of new phosphopeptides. We show that Nck, via its SH3 domains, specifically binds three major phosphoproteins of 95, 82 and 66 kDa both in vitro and in intact cells. Notably, the phosphorylation of these Nck-binding proteins was found to increase in parallel with that of Nck on stimulation by angiotensin II. One candidate for the 66 kDa phosphoprotein is the serine/threonine kinase p21-activated kinase 1 (Pak1), which was found to form a stable complex with Nck in aortic smooth muscle cells. We have also identified the gamma2 isoform of casein kinase I as another protein kinase that associates with Nck in these cells. These findings indicate that Nck is a target of G-protein-coupled receptors and suggest a role for Pak1 and casein kinase I-gamma2 in downstream signalling or regulation of the AT1 receptor.
Nck是一种小的衔接蛋白,仅由三个SH3结构域和一个SH2结构域组成。Nck被认为在细胞信号传导中发挥重要作用,它通过其SH2结构域将受体酪氨酸激酶与下游的SH3结合效应器偶联起来。我们在此报告,血管紧张素II通过AT1受体亚型发挥作用,刺激大鼠主动脉平滑肌细胞中Nck的磷酸化。磷酸肽图谱分析显示,在静止细胞中,Nck在仅含磷酸丝氨酸的四个肽段上被磷酸化。用血管紧张素II处理导致这四个肽段的磷酸化增加,且未出现新的磷酸肽段。我们表明,Nck通过其SH3结构域,在体外和完整细胞中均特异性结合95、82和66 kDa的三种主要磷蛋白。值得注意的是,在血管紧张素II刺激下,这些与Nck结合的蛋白的磷酸化与Nck的磷酸化平行增加。66 kDa磷蛋白的一个候选者是丝氨酸/苏氨酸激酶p21激活激酶1(Pak1),它在主动脉平滑肌细胞中与Nck形成稳定复合物。我们还鉴定出酪蛋白激酶I的γ2同工型是在这些细胞中与Nck结合的另一种蛋白激酶。这些发现表明Nck是G蛋白偶联受体的一个靶点,并提示Pak1和酪蛋白激酶I-γ2在AT1受体的下游信号传导或调节中发挥作用。