...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >PYK2 interacts with MyD88 and regulates MyD88-mediated NF-?oB activation in macrophages
【24h】

PYK2 interacts with MyD88 and regulates MyD88-mediated NF-?oB activation in macrophages

机译：PYK2与MyD88相互作用，并调节巨噬细胞中MyD88介导的NF-κB激活

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

PYK2, a major cell adhesion-activated tyrosine kinase, is highly expressed in macrophages and implicated in macrophage activation and inflammatory response. However, mechanisms by which PYK2 regulates inflammatory response are beginning to be understood. In this study, we demonstrate that PYK2 interacts with MyD88, a crucial signaling adaptor protein in LPS and PGN-induced NF-?oB activation, in vitro and in macrophages. This interaction, increased in macrophages, stimulated by LPS, requires the death domain of MyD88. PYK2-deficient macrophages exhibit reduced phosphorylation and degradation of I?oB, an inhibitor of NF-?oB nuclear translocation, and decreased NF-?oB activation and IL-1?2 expression by LPS. These results suggest that via interaction with MyD88, PYK2 is involved in modulating cytokine (e.g., LPS) stimulation of NF-?oB activity and signaling, providing a mechanism underlying PYK2 regulation of an inflammatory response.
机译：PYK2是一种主要的细胞粘附激活酪氨酸激酶，在巨噬细胞中高度表达，并与巨噬细胞激活和炎症反应有关。但是，人们开始了解PYK2调节炎症反应的机制。在这项研究中，我们证明了PYK2与MyD88相互作用，MyD88是体外和巨噬细胞中LPS和PGN诱导的NF-κB激活中的关键信号转导接头蛋白。这种相互作用在LPS刺激下在巨噬细胞中增加，需要MyD88的死亡域。缺乏PYK2的巨噬细胞显示IphoB（NF-κB核移位的抑制剂）的磷酸化和降解降低，并通过LPS降低NF-κB活化和IL-1β2表达。这些结果表明，通过与MyD88的相互作用，PYK2参与调节NF-κB活性和信号传导的细胞因子（例如，LPS）刺激，提供了炎症反应的PYK2调节基础的机制。

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