Green S L, Kulp K S, Vulliet R
Department of Molecular Biosciences, School of Veterinary, Medicine, University of California-Davis 95616, USA.
Neurochem Int. 1997 Oct;31(4):617-23. doi: 10.1016/s0197-0186(97)00012-0.
Cyclin-dependent kinase 5 (CDK5) is the 34 kDa catalytic subunit of a recently characterized neuronal cdc2-like protein kinase which appears to be involved in regulation of the neurocytoskeleton. Using the rat postdecapitative model, the effect of brain ischemia on histone H1 and tau protein CDK5 phosphorylating activity was examined. Histone H1 kinase activity increased in both cytosolic and particulate fractions of the hippocampus and neocortex after 5 min and 15 min of ischemia, then declined to control levels. CDK5 tau protein phosphorylating activity increased after 15 min ischemia; however, no electrophoretic shifts or changes in radiodensity of the tau bands were observed autoradiographically. On Western blot analysis, the CDK5 protein band did not change after 25 min ischemia, despite the increase and subsequent decline in enzyme activity. These data demonstrate a postischemic increase in CDK5 activity, an associated increase in CDK5 tau phosphorylating activity and a decline in activity in the absence of massive proteolysis. CDK5 appears to play a role in the events associated with neuronal response to ischemic injury.
细胞周期蛋白依赖性激酶5（CDK5）是一种最近被鉴定的神经元细胞周期蛋白依赖性激酶2样蛋白激酶的34 kDa催化亚基，它似乎参与神经细胞骨架的调节。利用大鼠断头后模型，研究了脑缺血对组蛋白H1和tau蛋白CDK5磷酸化活性的影响。缺血5分钟和15分钟后，海马体和新皮质的胞质和颗粒部分的组蛋白H1激酶活性均增加，然后降至对照水平。缺血15分钟后，CDK5 tau蛋白磷酸化活性增加；然而，放射自显影未观察到tau条带的电泳迁移或放射密度变化。蛋白质免疫印迹分析显示，尽管酶活性先增加后下降，但缺血25分钟后CDK5蛋白条带未发生变化。这些数据表明，缺血后CDK5活性增加，与之相关的CDK5 tau磷酸化活性增加，且在无大量蛋白质水解的情况下活性下降。CDK5似乎在与神经元对缺血性损伤反应相关的事件中起作用。
