Ohba Y
Laboratory of Molecular and Cellular Pathology, Department of Neurological Disorder, Division of Neurological Science, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Hokkaido Igaku Zasshi. 2001 Jan;76(1):13-20.
Rap2 is a member of Ras-family G proteins and related most closely to Rap1; however little is known about the regulation of Rap2 activity. In this study, I have compared the regulation and function of Rap2 with those of Rap1. In 293T cells, Rap2 was regulated by the same set of guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs) as those which regulated Rap1. Rap2 was localized at both plasma membrane and intracellular membrane compartments, as Rap1 was. Rap2 bound to the Ras-binding domain of Raf and inhibited Ras-dependent activation of Elk1 transcription factor. I have found that the GTP-bound form exceeds 50% of total Rap2 in the cells. This observation suggests that Rap2 suppresses Ras-mediated activation of ERK/MAP kinase cascade in quiescent cells.
Rap2是Ras家族G蛋白的成员，与Rap1关系最为密切；然而，关于Rap2活性的调节却知之甚少。在本研究中，我比较了Rap2与Rap1的调节和功能。在293T细胞中，Rap2受与调节Rap1相同的一组鸟嘌呤核苷酸交换因子（GEF）和GTP酶激活蛋白（GAP）的调节。与Rap1一样，Rap2定位于质膜和细胞内膜区室。Rap2与Raf的Ras结合结构域结合，并抑制Ras依赖的Elk1转录因子的激活。我发现细胞中GTP结合形式超过Rap2总量的50%。这一观察结果表明，Rap2在静止细胞中抑制Ras介导的ERK/MAP激酶级联反应的激活。
