• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >tau4/tau c/AF-2 of the thyroid hormone receptor relieves silencing of the retinoic acid receptor silencer core independent of both tau4 activation function and full dissociation of corepressors.
【24h】

tau4/tau c/AF-2 of the thyroid hormone receptor relieves silencing of the retinoic acid receptor silencer core independent of both tau4 activation function and full dissociation of corepressors.

机译：甲状腺激素受体的tau4 / tau c / AF-2减轻了视黄酸受体沉默子核心的沉默，而与tau4激活功能和核心加压因子的完全解离无关。

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

摘要

Members of the thyroid hormone (TR)-retinoic acid receptor (RAR) subfamily of nuclear hormone receptors silence gene expression in the absence of hormone. Addition of cognate ligands leads to dissociation of corepressors, association of coactivators, and transcriptional activation. Here, we used the hRAR alpha silencer core, which encompasses the ligand binding domain, including receptor regions D and E of RAR alpha without the activation function called tau4/tau c/AF-2 and without the F region, to analyze the mechanisms by which transcriptional silencing is relieved. Although the RAR silencer core is able to bind ligand, it acts as a constitutive transcriptional silencer. We have fused various small activation domains to the C terminus of the silencer core and analyzed hormone-dependent changes in receptor function. We show that nine amino acids derived from the hTRbeta are sufficient to transform the RAR silencer core into a hormone-dependent activator. Lengthening the linker between the silencer core and these nine amino acids is not critical for mediating ligand-induced relief of silencing and activation. In addition, we show that a transactivation function at the C terminus is not required for relief of silencing by the hormone, but it is required for transcriptional activation. Furthermore, we created functional silencer fusions which lose their repressive function upon addition of hormone, although the corepressors SMRT and N-CoR remain attached to the receptor.
机译：在没有激素的情况下，核激素受体的甲状腺激素（TR）-视黄酸受体（RAR）亚家族成员沉默基因表达。同源配体的添加导致共加压因子的解离，共激活因子的缔合和转录激活。在这里，我们使用了hRAR alpha沉默子核心（包括没有激活功能的tau4 / tau c / AF-2和F区域的RAR alpha的受体区域D和E，包括配体结合域）来分析机制，方法是转录沉默得以缓解。尽管RAR沉默子核心能够结合配体，但它可以作为组成型转录沉默子。我们已经将各种小的激活域融合到了沉默子核心的C末端，并分析了激素依赖性受体功能的变化。我们表明，从hTRbeta衍生的九个氨基酸足以将RAR沉默子核心转变为激素依赖性激活剂。延长沉默子核心和这9个氨基酸之间的连接子对于介导配体诱导的沉默和激活缓解并不关键。此外，我们表明，C末端的反式激活功能不是缓解激素沉默所必需的功能，而是转录激活所需的功能。此外，我们创建了功能性的消音融合体，尽管添加了荷尔蒙的辅助抑制剂SMRT和N-CoR仍然与受体结合，但它们失去了其抑制功能。

著录项

相似文献

  • 外文文献
  • 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