首页> 外文期刊>Cell Growth & Differentiation: The Molecular Biology Journal of the American Association for Cancer Research >Mechanism of induction of transforming growth factor-beta type II receptor gene expression by v-Src in murine myeloid cells.
【24h】

Mechanism of induction of transforming growth factor-beta type II receptor gene expression by v-Src in murine myeloid cells.

机译:v-Src在鼠骨髓细胞中诱导转化生长因子βII型受体基因表达的机制。

获取原文
获取原文并翻译 | 示例
           

摘要

Transforming growth factor (TGF)-beta1 plays an important role during hematopoiesis. Previously, we had shown that the growth of a v-Src-transformed myeloid cell line was markedly more inhibited by TGF-beta treatment when compared with the wild-type myeloid cell line. To investigate the increased growth sensitivity of the v-Src-transformed myeloid cell line, 32D-src, to TGF-beta, we examined expression of the TGF-beta type II receptor (TGF-beta RII) gene in myeloid cell lines. Northem blot analysis showed that expression of approximately 8- and 6-kb species of TGF-beta RII transcripts was markedly increased in the 32D-src cell line. The expression of the TGF-beta RII promoter linked to a reporter gene was increased 23-fold by v-Src. DNA transfection and electrophoretic mobility shift assay revealed that v-Src induces TGF-beta RII promoter activity through an AP1/ATF2-like sequence (-219 to -172), ETS binding sites (+1 to +36), and the inverted CCAAT box (-81 to -77). Novel DNA-protein complexes with ETS binding sites are significantly increased in v-src-transformed cell lines compared with the control cell line. These results suggest that v-Src induces activity of the TGF-beta RII promoter through multiple elements by inducing expression of nuclear proteins interacting with these elements.
机译:转化生长因子(TGF)-beta1在造血过程中起着重要作用。以前,我们已经表明,与野生型骨髓细胞系相比,TGF-β处理显着抑制了v-Src转化的骨髓细胞系的生长。为了研究v-Src转化的髓样细胞系32D-src对TGF-β增长的生长敏感性,我们检查了髓样细胞系中TGF-βII型受体(TGF-βRII)基因的表达。 Northem印迹分析表明,在32D-src细胞系中,约8和6 kb的TGF-βRII转录本的表达明显增加。与报告基因相连的TGF-βRII启动子的表达通过v-Src增加了23倍。 DNA转染和电泳迁移率变动分析表明,v-Src通过类AP1 / ATF2序列(-219至-172),ETS结合位点(+1至+36)和反向CCAAT诱导TGF-βRII启动子活性框(-81至-77)。与对照细胞系相比,在v-src转化的细胞系中,具有ETS结合位点的新型DNA-蛋白质复合物显着增加。这些结果表明,v-Src通过诱导与这些元件相互作用的核蛋白的表达,通过多种元件诱导TGF-βRII启动子的活性。

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