首页> 外文期刊>American Journal of Physiology >Tumor necrosis factor activates CRE-binding protein through a p38 MAPK/MSK1 signaling pathway in endothelial cells
【24h】

Tumor necrosis factor activates CRE-binding protein through a p38 MAPK/MSK1 signaling pathway in endothelial cells

机译:肿瘤坏死因子通过内皮细胞中的p38 MAPK / MSK1信号通路激活CRE结合蛋白

获取原文
获取原文并翻译 | 示例
           

摘要

Tumor necrosis factor (TNF) promotes immunity and modulates cell viability, in part, by promoting alterations of cellular gene expression. The mechanisms through which TNF communicates with the nucleus and alters gene expression are incompletely understood. Incubation of human umbilical vein endothelial cells (HUVEC) with TNF induces phosphoryla-tion of the CRE-binding protein (CREB) transcription factor on serine 133 and increases CREB DNA binding and transactivation. Dominant negative CREB, an antagonist antibody directed against the type 1 TNF receptor, or pharmacological inhibition of p38 MAPK signaling blocked TNF-induced CREB activation as determined by phosphor-ylation and gene reporter assays. From among the kinases that can activate CREB, we found that downstream of p38 MAPK, MSK1 is activated by TNF to promote CREB activation. These observations show that CREB is activated by TNF/TNFR1 signaling through a p38MAPK/MSKl signaling pathway.
机译:肿瘤坏死因子(TNF)部分通过促进细胞基因表达的改变而提高免疫力并调节细胞活力。 TNF与细胞核通讯并改变基因表达的机制尚不完全清楚。将人脐静脉内皮细胞(HUVEC)与TNF一起孵育可诱导丝氨酸133上CRE结合蛋白(CREB)转录因子的磷酸化,并增加CREB ​​DNA的结合和反式激活。显性阴性CREB,针对1型TNF受体的拮抗抗体或p38 MAPK信号的药理抑制作用可阻断TNF诱导的CREB活化,如磷酸化和基因报告基因检测所确定。在可以激活CREB的激酶中,我们发现p38 MAPK的下游,MSK1被TNF激活以促进CREB激活。这些观察结果表明CREB被TNF / TNFR1信号通过p38MAPK / MSK1信号通路激活。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号