Ramaswamy N T, Ronai Z, Pelling J C
Department of Pathology, University of Kansas Medical Center, Kansas City 66160-7410, USA.
Oncogene. 1998 Mar;16(11):1501-5. doi: 10.1038/sj.onc.1201628.
Jun N-terminal kinase (JNK1) is a member of a family of stress-activated protein kinases which are activated by many forms of stress including UV radiation, resulting in the phosphorylation of c-Jun, ATF-2, Elk-1 and p53. As UV-B radiation is mainly responsible for ultraviolet (UV)-induced skin cancers, we chose to elucidate JNK1 activation in keratinocytes which represent a UV-relevant cell system. We have demonstrated rapid activation of JNK1 in a keratinocyte cell line, C50, in response to multiple doses of UV-B irradiation. JNK1 activation occurred within 1 min, peaked by 10 min and returned to near basal levels within 2 h following the UV-B treatments. Our data provide the first evidence to show that keratinocytes do respond to multiple doses of the physiologically relevant UV-B radiation through rapid activation of the JNK1 pathway.
Jun氨基末端激酶（JNK1）是应激激活蛋白激酶家族的成员之一，该家族可被多种形式的应激激活，包括紫外线辐射，从而导致c-Jun、ATF-2、Elk-1和p53的磷酸化。由于UV-B辐射是紫外线（UV）诱导皮肤癌的主要原因，我们选择阐明角质形成细胞中JNK1的激活情况，角质形成细胞代表了一个与紫外线相关的细胞系统。我们已经证明，在角质形成细胞系C50中，JNK1可对多剂量的UV-B照射作出快速激活反应。JNK1的激活在1分钟内发生，10分钟时达到峰值，并在UV-B处理后2小时内恢复到接近基础水平。我们的数据首次证明，角质形成细胞确实通过JNK1途径的快速激活对多剂量的生理相关UV-B辐射作出反应。
