Ludwig S, Hoffmeyer A, Goebeler M, Kilian K, Häfner H, Neufeld B, Han J, Rapp U R
Institut für Medizinische Strahlenkunde und Zellforschung (MSZ), University of Würzburg, Germany.
J Biol Chem. 1998 Jan 23;273(4):1917-22. doi: 10.1074/jbc.273.4.1917.
Cell response to a wide variety of extracellular signals is mediated by either mitogenic activation of the Raf/MEK/ERK kinase cascade or stress-induced activation of the mitogen-activated protein kinase (MAPK) family members c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) or p38. We have examined communications between these stress- and mitogen-induced signaling pathways. We show here that the stress cascade activator arsenite activates extracellular signal-regulated kinase (ERK) in addition to p38 albeit with different kinetics. Whereas p38 is an early response kinase, ERK activation occurs with delayed time kinetics at 2-4 h. We observed activation of ERK upon arsenite treatment in many different cell lines. ERK activation is strongly enhanced by overexpression of p38 and mitogen-activated protein kinase kinase 6 (MKK6) but is blocked by dominant negative kinase versions of p38 and MKK6 or the specific p38 inhibitor SB203580. Arsenite-induced ERK activation is mediated by Ras, Raf, and MEK but appears to be independent of de novo protein synthesis. These data provide the first evidence for a p38 dependent activation of the mitogenic kinase cascade in stress-stimulated cells.
细胞对多种细胞外信号的反应是由Raf/MEK/ERK激酶级联的促有丝分裂激活或应激诱导的丝裂原活化蛋白激酶(MAPK)家族成员c-Jun氨基末端激酶/应激激活蛋白激酶(JNK/SAPK)或p38的激活介导的。我们研究了这些应激和促有丝分裂诱导的信号通路之间的通讯。我们在此表明,应激级联激活剂亚砷酸盐除了激活p38外,还能激活细胞外信号调节激酶(ERK),尽管其动力学不同。p38是一种早期反应激酶,而ERK的激活在2-4小时时呈现延迟的时间动力学。我们在许多不同的细胞系中观察到亚砷酸盐处理后ERK的激活。p38和丝裂原活化蛋白激酶激酶6(MKK6)的过表达强烈增强了ERK的激活,但p38和MKK6的显性负性激酶变体或特异性p38抑制剂SB203580可阻断这种激活。亚砷酸盐诱导的ERK激活由Ras、Raf和MEK介导,但似乎与从头合成蛋白质无关。这些数据为应激刺激细胞中有丝分裂激酶级联的p38依赖性激活提供了首个证据。