缺血/再灌注损伤时丝裂原活化蛋白激酶信号转导通路的变化  

Changes of mitogen-activated protein kinases signal transduction pathway in ischemia/reperfusion injury

作　　者：蔡琪[1] 李晓玫[1] 王海燕[1] 

机构地区：[1]北京医科大学第一医院肾内科暨肾脏病研究所,北京100034

出　　处：《中国病理生理杂志》2000年第12期1335-1337,共3页Chinese Journal of Pathophysiology

基　　金：教育部博士学科点基金! (No .95 0 10 2 9)

摘　　要：Mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERKs), c-Jun NH2-terminal kinases (JNKs) and p38 MAPK, play an important role in transducting environmental stimuli to the transcriptional machinery in the nucleus in mammalian cells by virtue of their ability to phosphorylate and regulate the activity of various transcription factors. It was recently found that the changes in activity of MAPKs occurred during ischemia/reperfusion, but the biological significance of the changes was still controversial.Mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERKs), c-Jun NH2-terminal kinases (JNKs) and p38 MAPK, play an important role in transducting environmental stimuli to the transcriptional machinery in the nucleus in mammalian cells by virtue of their ability to phosphorylate and regulate the activity of various transcription factors. It was recently found that the changes in activity of MAPKs occurred during ischemia/reperfusion, but the biological significance of the changes was still controversial.

关 键 词：局部缺血 再灌注损伤 有丝分裂原 蛋白激酶 

分 类 号：R364.1[医药卫生—病理学]