• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Signalling >Lyn contributes to regulation of multiple Kit-dependent signaling pathways in murine bone marrow mast cells
【24h】

Lyn contributes to regulation of multiple Kit-dependent signaling pathways in murine bone marrow mast cells

机译：Lyn有助于调节小鼠骨髓肥大细胞中多种Kit依赖的信号通路

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

SCF induces autophosphorylation of Kit and activates a variety of signaling components including Jnks, Erks, PI 3 Kinase, the JAK-Stat pathway and members of the Src family. Previously we showed that Lyn is activated at multiple points during SCF-induced cell cycle progression and contributes to SCF-mediated growth, chemotaxis and internalization of Kit. However, the Kit-dependent biochemical events that require Lyn are unknown. In this study, we used Lyn-deficient bone marrow mast cells (BMMC) to examine the contribution of this Src family member to tyrosine phosphorylation of Kit and SCF-induced activation of Jnks, Akt, Stat3 and Erks. Although surface expression of Kit was increased in Lyn-deficient BMMC, SCF-induced phosphorylation and growth was reduced compared to wild-type BMMC. Downstream of Kit, SCF-induced activation of Jnks was markedly reduced in Lyn-deficient BMMC. Further, Lyn was required for SCF-induced tyrosine phosphorylation of Stat3. Interestingly, Kit was constitutively associated with PI 3 Kinase in Lyn-deficient BMMC and this correlated with constitutive phosphorylation of Akt. This was in marked contrast to wild-type BMMC, where both these events were induced by SCF. These data indicate that in BMMC, Lyn contributes to SCF-induced phosphorylation of Kit, as well as phosphorylation of Jnks and Stat3. In contrast, Lyn may negatively regulate the PI 3 Kinase/Akt pathway. The opposing effects of Lyn on these signaling pathways may explain the pleiotropic effects ascribed to this Src family member in the literature. (C) 2004 Elsevier Inc. All rights reserved.
机译：SCF诱导Kit的自磷酸化并激活各种信号转导成分，包括Jnks，Erks，PI 3激酶，JAK-Stat途径和Src家族的成员。先前，我们显示Lyn在SCF诱导的细胞周期进程中在多个点被激活，并有助于SCF介导的Kit的生长，趋化性和内在化。但是，需要Lyn的试剂盒依赖性生化事件尚不清楚。在这项研究中，我们使用Lyn缺陷型骨髓肥大细胞（BMMC）来检查该Src家族成员对Kit酪氨酸磷酸化和SCF诱导的Jnks，Akt，Stat3和Erks活化的贡献。尽管Kit的表面表达在Lyn缺陷BMMC中增加，但与野生型BMMC相比，SCF诱导的磷酸化和生长减少。在Kit的下游，Lyn缺陷BMMC中SCF诱导的Jnks激活显着减少。此外，SCF诱导的Stat3酪氨酸磷酸化需要Lyn。有趣的是，Kit与Lyn缺陷BMMC中的PI 3激酶组成性相关，并且与Akt的组成型磷酸化相关。这与野生型BMMC形成鲜明对比，在野生型BMMC中，这两个事件都是由SCF诱导的。这些数据表明，在BMMC中，Lyn有助于SCF诱导的Kit磷酸化，以及Jnks和Stat3的磷酸化。相反，Lyn可能会对PI 3激酶/ Akt通路产生负面影响。 Lyn对这些信号通路的相反作用可能解释了文献中归因于该Src家族成员的多效作用。 （C）2004 Elsevier Inc.保留所有权利。

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