Mammalian MAPK Signal Transduction Pathways Activated by Stress and Inflammation: A 10-Year Update

MAPK/ERK通路 激酶 生物 信号转导 细胞生物学 炎症 基因剔除小鼠 癌变 丝裂原活化蛋白激酶 神经科学 计算生物学 免疫学 癌症 遗传学 受体
作者
John Kyriakis,Joseph Avruch
出处
期刊:Physiological Reviews [American Physiological Society]
卷期号:92 (2): 689-737 被引量:1229
标识
DOI:10.1152/physrev.00028.2011
摘要

The mammalian stress-activated families of mitogen-activated protein kinases (MAPKs) were first elucidated in 1994, and by 2001, substantial progress had been made in identifying the architecture of the pathways upstream of these kinases as well as in cataloguing candidate substrates. This information remains largely sound. Nevertheless, an informed understanding of the physiological and pathophysiological roles of these kinases remained to be accomplished. In the past decade, there has been an explosion of new work using RNAi in cells, as well as transgenic, knockout and conditional knockout technology in mice that has provided valuable insight into the functions of stress-activated MAPK pathways. These findings have important implications in our understanding of organ development, innate and acquired immunity, and diseases such as atherosclerosis, tumorigenesis, and type 2 diabetes. These new developments bring us within striking distance of the development and validation of novel treatment strategies. Herein we first summarize the molecular components of the mammalian stress-regulated MAPK pathways and their regulation as described thus far. We then review some of the in vivo functions of these pathways.
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