...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Estradiol rapidly regulates membrane estrogen receptor alpha levels in hypothalamic neurons.
【24h】

Estradiol rapidly regulates membrane estrogen receptor alpha levels in hypothalamic neurons.

机译：雌二醇快速调节下丘脑神经元中的膜雌激素受体α水平。

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

Estrogen receptors (ERs) and estrogen-binding proteins have been localized intracellularly and on the cell surface. The membrane-associated proteins initiate signaling that activates a myriad of cellular responses including the modulation of ion channels and ultimately transcription. Although many of the downstream actions of membrane ERs, including ERalpha and ERbeta, have been characterized, the mechanisms regulating membrane ER levels have remained elusive in the nervous system. In the present study, we used surface biotinylation to identify and study the estradiol regulation of membrane ERalpha in mixed-sex, cultured hypothalamic neurons from rat. Following surface biotinylation, Western blot analysis revealed full-length 66 kDa ERalpha and several ERalpha splice variants, most notably a biotinylated 52 kDa ERalpha-immunoreactive protein. Treatment of the neurons with estradiol caused a rapid and transient increase of the biotinylated 52 kDa and 66 kDa ERalpha proteins in the plasma membrane. Exposure of the neurons to estradiol also significantly increased internalization of 52 kDa and 66 kDa ERalpha membrane proteins, a measure of receptor activation. In the hypothalamus, membrane ERalpha signaling depends on transactivation of metabotropic glutamate receptor-1a (mGluR1a). Estradiol treatment increased the internalization of mGluR1a in parallel with ERalpha, a finding consistent with the hypothesis of an ERalpha-mGluR1a signaling unit. These results demonstrate that estradiol regulates the amount of ERalpha in the membrane, suggesting estradiol can regulate its own membrane signaling.
机译：雌激素受体（ERs）和雌激素结合蛋白已定位在细胞内和细胞表面。膜相关蛋白启动信号传导，激活多种细胞反应，包括调节离子通道和最终转录。尽管已表征了膜内质网的许多下游作用，包括ERalpha和ERbeta，但调节膜内质网水平的机制在神经系统中仍然难以捉摸。在本研究中，我们使用表面生物素化来鉴定和研究雌性大鼠混合性下丘脑神经元中膜ERalpha的雌二醇调节。表面生物素化后，蛋白质印迹分析显示全长66 kDa ERalpha和几个ERalpha剪接变体，最著名的是生物素化的52 kDa ERalpha免疫反应蛋白。用雌二醇处理神经元导致质膜中生物素化的52 kDa和66 kDa ERalpha蛋白迅速而短暂地增加。将神经元暴露于雌二醇也显着增加了52 kDa和66 kDa ERalpha膜蛋白的内在化，这是受体激活的一种度量。在下丘脑中，膜ERalpha信号依赖于代谢型谷氨酸受体1a（mGluR1a）的反式激活。雌二醇治疗与ERalpha并行增加了mGluR1a的内在化，这一发现与ERalpha-mGluR1a信号单元的假设一致。这些结果表明，雌二醇调节膜中ERα的量，表明雌二醇可以调节其自身的膜信号传导。

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