...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Oncogenic Met receptor induces cell-cycle progression in Xenopus oocytes independent of direct Grb2 and Shc binding or Mos synthesis, but requires phosphatidylinositol 3-kinase and Raf signaling.
【24h】

Oncogenic Met receptor induces cell-cycle progression in Xenopus oocytes independent of direct Grb2 and Shc binding or Mos synthesis, but requires phosphatidylinositol 3-kinase and Raf signaling.

机译：致癌满足受体诱发细胞循环进展在非洲爪蟾蜍卵母细胞的独立人体自燃现象直接Grb2和绑定或金属氧化物半导体的合成,但需要磷脂酰肌醇3-kinase和英国皇家空军信号。

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

摘要

Biological responses of hepatocyte growth factor (HGF) are mediated by the Met receptor tyrosine kinase. Although HGF is a potent mitogen for a variety of cells, the signals required for cell-cycle progression by the Met/HGF receptor are poorly defined. In this study, we have used the Xenopus oocyte system to define the role of various Met proximal-binding partners and downstream signaling pathways in cell-cycle regulation. We show that cell-cycle progression and activation of MAPK and JNK mediated by the oncogenic Met receptor, Tpr-Met, are dependent on its kinase activity and the presence of the twin phosphotyrosine (Y482 & Y489) residues in its C-terminus, but that the recruitment of Grb2 and Shc adaptor proteins is dispensable, implicating other signaling molecules. However, using Met receptor oncoproteins engineered to recruit specific signaling proteins, we demonstrate that recruitment of Grb2 or Shc adaptor proteins is sufficient to induce cell-cycle progression and activation of MAPK and JNK, while the binding of phospholipase-Cgamma or phosphatidylinositol 3-kinase alone fails to elicit these responses. Using various means to block phosphatidylinositol 3-kinase, phospholipase-Cgamma, MEK, JNK, Mos, and Raf1 activity, we show that unlike the fibroblast growth factor receptor, MEK-dependent and independent signaling contribute to Met receptor-mediated cell-cycle progression, but phospholipase-Cgamma or JNK activity and Mos synthesis are not critical. Notably, we demonstrate that Raf1 and phosphatidylinositol 3-kinase signaling are required for cell-cycle progression initiated by the Met receptor, a protein frequently deregulated in human tumors.
机译：肝细胞生长因子的生物学反应(HGF)介导的受体酪氨酸激酶。各种各样的细胞,所需的信号满足/ HGF受体细胞循环发展不定义。非洲爪蟾蜍的卵母细胞系统定义的角色各种proximal-binding伙伴和见面下游信号通路在细胞循环监管。和激活MAPK和物介导的致癌受体,Tpr-Met依赖其激酶活性和双胞胎的存在phosphotyrosine (Y482 & Y489)残留的糖基,但招聘Grb2和自燃适配器蛋白质是可有可无的,暗示其他信号分子。受体癌基因蛋白工程招聘特定的信号蛋白,我们证明招聘Grb2人体自燃现象或适配器蛋白质足以诱导细胞循环发展激活MAPK和物,而绑定的phospholipase-Cgamma或磷脂酰肌醇独自3-kinase未能引起这些反应。使用各种手段阻碍磷脂酰肌醇3-kinase phospholipase-Cgamma, MEK物,金属氧化物半导体,和Raf1活动,我们表明,不同纤维母细胞生长因子受体,MEK-dependent和独立的信号有助于满足受体介导细胞循环发展,但是phospholipase-Cgamma或物活动和金属氧化物半导体合成并不是最关键的。证明Raf1和磷脂酰肌醇3-kinase信号所需细胞循环进展由大都会受体在人类肿瘤蛋白质经常管制。

著录项

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