...
首页> 外文期刊>American Journal of Physiology >Focal adhesion kinase phosphorylation in flow-activation of endothelial NF-kB. Focus on 'Focal adhesion kinase modulates activation of NF-kB by flow in endothelial cells'
【24h】

Focal adhesion kinase phosphorylation in flow-activation of endothelial NF-kB. Focus on 'Focal adhesion kinase modulates activation of NF-kB by flow in endothelial cells'

机译:内皮NF-Kb流动激活中的焦粘激酶磷酸化。 专注于“局灶性粘附激酶通过内皮细胞流动调节NF-Kb的活化”

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

in this issue of American Journal of Physiology-Cell Physiology, Petzold et al. (corresponding author Martin A. Schwartz) report their results from a very interesting study, "Focal adhesion kinase modulates activation of NF-kB by flow in endothelial cells" (10). Comparing endothelial cells (ECs) from mice with a floxed focal adhesion kinase (FAK) gene (FAK~(fl/fl)) and those with cre-deletion knockout (FAK~(-/-)), these authors were able to assess the role of FAK in the activation of NF-kB in ECs. They report the novel finding that FAK is indispensible for the flow-induced phosphorylation of NF-kB at Ser536 and the expression of downstream proinflammatory molecules, but not for the flow-induced nuclear translocation of the p65 subunit of NF-kB following IkB degradation, which is generally considered to be a key event in the activation of NF-kB and its downstream molecules.
机译:在这个美国生理学 - 细胞生理学杂志中,Petzold等人。 (相应的作者Martin A. Schwartz)从一个非常有趣的研究报告它们的结果,“局灶性粘合激酶通过内皮细胞流动调节NF-Kb的活化”(10)。 将内皮细胞(ECS)与含有碳焦粘连激酶(FAK)基因(FFAK〜(FL / FL))和Cre-Deletion敲除(FAK〜( - / - ))的小鼠进行比较,这些作者能够评估 FAK在ECS中NF-KB激活中的作用。 他们报告了新颖的发现,FAK在SER536中的NF-KB的流动诱导的磷酸化和下游促炎分子的表达,但不用于IKB降解后NF-KB的P65亚基的流动诱导的核易位, 通常认为是NF-KB的激活和下游分子中的关键事件。

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