Procyk K J, Kovarik P, von Gabain A, Baccarini M
Department of Cell and Microbiology, Institute of Microbiology and Genetics, Vienna Biocenter, 1030 Vienna, Austria.
Infect Immun. 1999 Mar;67(3):1011-7. doi: 10.1128/IAI.67.3.1011-1017.1999.
Activation of the extracellularly regulated kinase (ERK) pathway is part of the early biochemical events that follow lipopolysaccharide (LPS) treatment of macrophages or their infection by virulent and attenuated Salmonella strains. Phagocytosis as well as the secretion of invasion-associated proteins is dispensable for ERK activation by the pathogen. Furthermore, the pathways used by Salmonella and LPS to stimulate ERK are identical, suggesting that kinase activation might be solely mediated by LPS. Both stimuli activate ERK by a mechanism involving herbimycin-dependent tyrosine kinase(s) and phosphatidylinositol 3-kinase. Phospholipase D activation and stimulation of protein kinase C appear to be intermediates in this novel pathway of MEK/ERK activation.
细胞外调节激酶(ERK)途径的激活是巨噬细胞经脂多糖(LPS)处理或被强毒和减毒沙门氏菌菌株感染后早期生化事件的一部分。病原体激活ERK无需吞噬作用以及侵袭相关蛋白的分泌。此外,沙门氏菌和LPS刺激ERK所使用的途径相同,这表明激酶激活可能仅由LPS介导。两种刺激均通过涉及除草霉素依赖性酪氨酸激酶和磷脂酰肌醇3激酶的机制激活ERK。磷脂酶D的激活和蛋白激酶C的刺激似乎是MEK/ERK激活这一新途径的中间环节。