• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell Research >Modulation of the activation of Stat1 by the interferon-gamma receptor complex.
【24h】

Modulation of the activation of Stat1 by the interferon-gamma receptor complex.

机译：干扰素-γ受体复合物对Stat1激活的调节。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The activation of Stat1 by the interferon-gamma (IFN-gamma) receptor complex is responsible for the transcription of a significant portion of IFN-gamma induced genes. Many of these genes are responsible for the induction of an apoptotic state in response to IFN-gamma. In the absence of Stat1 activation, IFN-gamma instead induces a proliferative response. Modifying Stat1 activation by IFN-gamma may have pharmacological benefits. We report that the rate of activation of Stat1 can be altered in HeLa cells by overexpressing either the IFN-gammaR1 chain or the IFN-gammaR2 chain. These alterations occur in hematopoietic cell lines: Raji cells and monocytic cell lines, which have average and above-average IFN-gammaR2 surface expression, activate Stat1 similarly to HeLa cells and HeLa cells overexpressing IFNgammaR2, respectively. The rapid Stat1 activation seen in HeLa cells can be inhibited by overexpressing a chimeric IFN-gammaR2 chain that does not bind Jak2 or (when high concentrations of IFN-gamma are used) by overexpressing IFN-gammaR1. These data are consistent with a model in which the recruitment of additional Jak2 activity to a signaling complex accelerates the rate of Stat1 activation. We conclude that the rate of activation of Stat1 in cells by IFN-gamma can be modified by regulating either receptor chain and speculate that pharmacological agents which modify receptor chain expression may alter IFN-gamma receptor signal transduction.Cell Research (2006) 16: 113-123. doi:10.1038/sj.cr.7310015; published online 16 January 2006.
机译：干扰素-γ（IFN-γ）受体复合物对Stat1的激活负责大部分IFN-γ诱导基因的转录。这些基因中的许多负责响应IFN-γ诱导凋亡状态。在没有Stat1激活的情况下，IFN-γ会诱导增殖反应。通过IFN-γ修饰Stat1激活可能具有药理学益处。我们报告说，Stat1的激活率可以通过过表达IFN-gammaR1链或IFN-gammaR2链而在HeLa细胞中改变。这些改变发生在造血细胞系中：具有平均和高于平均水平的IFN-gammaR2表面表达的Raji细胞和单核细胞系分别激活Stat1，类似于激活IFNgammaR2的HeLa细胞和HeLa细胞。在HeLa细胞中看到的快速Stat1激活可以通过过表达不与Jak2结合的嵌合IFN-gammaR2链来抑制，或者通过过表达IFN-gammaR1来抑制（当使用高浓度的IFN-γ时）。这些数据与一个模型一致，在该模型中，向信号复合物募集额外的Jak2活性可加快Stat1激活的速率。我们得出的结论是，可以通过调节任一受体链来修饰IFN-γ在细胞中激活Stat1的速率，并推测修饰受体链表达的药理剂可能会改变IFN-γ受体的信号转导.Cell Research（2006）16：113 -123。 doi：10.1038 / sj.cr.7310015;在线发布于2006年1月16日。

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