Bivona Trever G, Pérez De Castro Ignacio, Ahearn Ian M, Grana Theresa M, Chiu Vi K, Lockyer Peter J, Cullen Peter J, Pellicer Angel, Cox Adrienne D, Philips Mark R
Department of Medicine, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA.
Nature. 2003 Aug 7;424(6949):694-8. doi: 10.1038/nature01806. Epub 2003 Jun 29.
Ras proteins regulate cellular growth and differentiation, and are mutated in 30% of cancers. We have shown recently that Ras is activated on and transmits signals from the Golgi apparatus as well as the plasma membrane but the mechanism of compartmentalized signalling was not determined. Here we show that, in response to Src-dependent activation of phospholipase Cgamma1, the Ras guanine nucleotide exchange factor RasGRP1 translocated to the Golgi where it activated Ras. Whereas Ca(2+) positively regulated Ras on the Golgi apparatus through RasGRP1, the same second messenger negatively regulated Ras on the plasma membrane by means of the Ras GTPase-activating protein CAPRI. Ras activation after T-cell receptor stimulation in Jurkat cells, rich in RasGRP1, was limited to the Golgi apparatus through the action of CAPRI, demonstrating unambiguously a physiological role for Ras on Golgi. Activation of Ras on Golgi also induced differentiation of PC12 cells, transformed fibroblasts and mediated radioresistance. Thus, activation of Ras on Golgi has important biological consequences and proceeds through a pathway distinct from the one that activates Ras on the plasma membrane.
Ras蛋白调节细胞生长和分化,在30%的癌症中发生突变。我们最近发现,Ras在高尔基体以及质膜上被激活并传递信号,但信号分隔的机制尚未确定。在这里我们表明,响应于Src依赖的磷脂酶Cγ1激活,Ras鸟嘌呤核苷酸交换因子RasGRP1易位至高尔基体,在那里它激活了Ras。虽然Ca(2+)通过RasGRP1正向调节高尔基体上的Ras,但相同的第二信使通过Ras GTP酶激活蛋白CAPRI负向调节质膜上的Ras。在富含RasGRP1的Jurkat细胞中,T细胞受体刺激后Ras的激活通过CAPRI的作用局限于高尔基体,明确证明了Ras在高尔基体上的生理作用。高尔基体上Ras的激活还诱导了PC12细胞的分化、转化成纤维细胞并介导了放射抗性。因此,高尔基体上Ras的激活具有重要的生物学后果,并且通过一条不同于激活质膜上Ras的途径进行。