Wu J, Dent P, Jelinek T, Wolfman A, Weber M J, Sturgill T W
Department of Internal Medicine, University of Virginia, Health Sciences Center, Charlottesville 22908.
Science. 1993 Nov 12;262(5136):1065-9. doi: 10.1126/science.7694366.
Mitogen-activated protein (MAP) kinases p42mapk and p44mapk are activated in cells stimulated with epidermal growth factor (EGF) and other agents. A principal pathway for MAP kinase (MAPK) activation by EGF consists of sequential activations of the guanine nucleotide exchange factor Sos, the guanosine triphosphate binding protein Ras, and the protein kinases Raf-1, MAPK kinase (MKK), and MAPK. Because adenosine 3',5'-monophosphate (cAMP) does not activate MAPK and has some opposing physiologic effects, the effect of increasing intracellular concentrations of cAMP with forskolin and 3-isobutyl-1-methylxanthine on the EGF-stimulated MAPK pathway was studied. Increased concentrations of cAMP blocked activation of Raf-1, MKK, and MAPK in Rat1hER fibroblasts, accompanied by a threefold increase in Raf-1 phosphorylation on serine 43 in the regulatory domain. Phosphorylation of Raf-1 in vitro and in vivo reduces the apparent affinity with which it binds to Ras and may contribute to the blockade by cAMP.
丝裂原活化蛋白(MAP)激酶p42mapk和p44mapk在受到表皮生长因子(EGF)及其他因子刺激的细胞中被激活。EGF激活MAP激酶(MAPK)的主要途径包括鸟嘌呤核苷酸交换因子Sos、鸟苷三磷酸结合蛋白Ras以及蛋白激酶Raf-1、MAPK激酶(MKK)和MAPK的依次激活。由于3',5'-环磷酸腺苷(cAMP)不激活MAPK且具有一些相反的生理效应,因此研究了用毛喉素和3-异丁基-1-甲基黄嘌呤增加细胞内cAMP浓度对EGF刺激的MAPK途径的影响。cAMP浓度升高会阻断大鼠1hER成纤维细胞中Raf-1、MKK和MAPK的激活,同时调节域中丝氨酸43处的Raf-1磷酸化增加了三倍。体外和体内Raf-1的磷酸化会降低其与Ras结合的表观亲和力,这可能是cAMP产生阻断作用的原因。