Adler V, Yin Z, Tew K D, Ronai Z
Ruttenberg Cancer Center, Mount Sinai School of Medicine, 1 Gustave Levy Place, Box 1130, New York, NY 10029, USA.
Oncogene. 1999 Nov 1;18(45):6104-11. doi: 10.1038/sj.onc.1203128.
Stress-activated signaling cascades are affected by altered redox potential. Key contributors to altered redox potential are reactive oxygen species (ROS) which are formed, in most cases, by exogenous genotoxic agents including irradiation, inflammatory cytokines and chemical carcinogens. ROS and altered redox potential can be considered as the primary intracellular changes which regulate protein kinases, thereby serving as an important cellular component linking external stimuli with signal transduction in stress response. The mechanisms, which underlie the ROS-mediated response, involve direct alteration of kinases and transcription factors, and indirect modulation of cysteine-rich redox-sensitive proteins exemplified by thioredoxin and glutathione S-transferase. This review summarizes the current understanding of the mechanisms contributing to ROS-related changes in key stress activated signaling cascades.
应激激活的信号级联反应受氧化还原电位改变的影响。氧化还原电位改变的主要促成因素是活性氧（ROS），在大多数情况下，活性氧由包括辐射、炎性细胞因子和化学致癌物在内的外源性基因毒性剂形成。ROS和氧化还原电位改变可被视为调节蛋白激酶的主要细胞内变化，从而作为将外部刺激与应激反应中的信号转导联系起来的重要细胞成分。ROS介导的反应所依据的机制涉及激酶和转录因子的直接改变，以及以硫氧还蛋白和谷胱甘肽S-转移酶为例的富含半胱氨酸的氧化还原敏感蛋白的间接调节。本综述总结了目前对关键应激激活信号级联反应中与ROS相关变化的机制的理解。
