Gotoh I, Adachi M, Nishida E
Department of Biophysics, Graduate School of Science, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan.
J Biol Chem. 2001 Feb 9;276(6):4276-86. doi: 10.1074/jbc.M008595200. Epub 2000 Oct 19.
The MAPK cascades regulate a wide variety of cellular functions, including cell proliferation, differentiation, and stress responses. Here we have identified a novel MAP kinase kinase kinase (MAPKKK), termed MLTK (for MLK-like mitogen-activated protein triple kinase), whose expression is increased by activation of the ERK/MAPK pathway. There are two alternatively spliced forms of MLTK, MLTKalpha and MLTKbeta. When overexpressed in cells, both MLTKalpha and MLTKbeta are able to activate the ERK, JNK/SAPK, p38, and ERK5 pathways. Moreover, both MLTKalpha and MLTKbeta are activated in response to osmotic shock with hyperosmolar media through autophosphorylation. Remarkably, expression of MLTKalpha, but not MLTKbeta, in Swiss 3T3 cells results in the disruption of actin stress fibers and dramatic morphological changes. A kinase-dead form of MLTKalpha does not cause these phenomena. Inhibition of the p38 pathway significantly blocks MLTKalpha-induced stress fiber disruption and morphological changes. These results suggest that MLTK is a stress-activated MAPKKK that may be involved in the regulation of actin organization.
丝裂原活化蛋白激酶(MAPK)级联反应调控多种细胞功能,包括细胞增殖、分化及应激反应。在此,我们鉴定出一种新型的丝裂原活化蛋白激酶激酶激酶(MAPKKK),命名为MLTK(类MLK丝裂原活化蛋白三联激酶),其表达可通过ERK/MAPK途径的激活而增加。MLTK有两种可变剪接形式,即MLTKα和MLTKβ。当在细胞中过表达时,MLTKα和MLTKβ均能激活ERK、JNK/SAPK、p38和ERK5途径。此外,MLTKα和MLTKβ在高渗培养基诱导的渗透压休克刺激下,均可通过自身磷酸化被激活。值得注意的是,在瑞士3T3细胞中表达MLTKα而非MLTKβ会导致肌动蛋白应力纤维的破坏及显著的形态学改变。MLTKα的激酶失活形式不会引发这些现象。抑制p38途径可显著阻断MLTKα诱导的应力纤维破坏及形态学改变。这些结果表明,MLTK是一种应激激活的MAPKKK,可能参与肌动蛋白组织的调控。