...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Liver-specific mRNA for Insig-2 down-regulated by insulin: implications for fatty acid synthesis.
【24h】

Liver-specific mRNA for Insig-2 down-regulated by insulin: implications for fatty acid synthesis.

机译：Insig-2的肝脏特异性mRNA被胰岛素下调：对脂肪酸合成的影响。

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

Insig-1 and -2 are closely related proteins of the endoplasmic reticulum (ER) that block proteolytic activation of sterol regulatory element-binding proteins (SREBPs), transcription factors that activate the synthesis of cholesterol and fatty acids in liver and other organs. When cellular cholesterol levels are high, Insig proteins bind and trap SREBP cleavage-activating protein (SCAP), retaining it in the ER and preventing it from escorting SREBPs from ER to the site of proteolytic activation in the Golgi complex. Here, we report the discovery of a liver-specific transcript of Insig-2, designated Insig-2a. This transcript and the ubiquitous transcript, designated Insig-2b, differ through the use of different promoters that produce different noncoding first exons that splice into a common second exon. Although the Insig-2a and -2b mRNAs encode identical proteins, they differ in patterns of regulation. Insig-2a is the predominant transcript in livers of fed animals, and it is selectively down-regulated by insulin. Insig-2a mRNA increases when mice are fasted, and it declines when they are refed. The transcript also increases in livers of rats whose insulin-secreting pancreatic beta cells have been destroyed by streptozotocin, and it is reduced when insulin is injected. The insulin-mediated fall in Insig-2a may allow SREBP-1c to be processed, thereby allowing insulin to stimulate fatty acid synthesis, even under conditions in which hepatic cholesterol levels are elevated.
机译：Insig-1和-2是内质网（ER）的紧密相关蛋白，可阻止固醇调节元件结合蛋白（SREBPs）的蛋白水解活化，而SREBPs是激活肝脏和其他器官中胆固醇和脂肪酸合成的转录因子。当细胞胆固醇水平高时，Insig蛋白会结合并捕获SREBP裂解激活蛋白（SCAP），将其保留在ER中并阻止其将SREBPs从ER护送到高尔基体中的蛋白水解激活位点。在这里，我们报告发现称为Insig-2a的Insig-2肝脏特异性转录本的发现。此转录本和普遍存在的转录本称为Insig-2b，通过使用不同的启动子来产生差异，这些启动子会产生不同的非编码第一外显子，并剪接到一个共同的第二外显子上。尽管Insig-2a和-2b mRNA编码相同的蛋白质，但是它们的调控方式不同。 Insig-2a是被摄食动物肝脏中的主要转录物，它被胰岛素选择性地下调。禁食小鼠时，Insig-2a mRNA增加，而当小鼠禁食时，Insig-2a mRNA则下降。胰岛素分泌的胰腺β细胞已被链脲佐菌素破坏的大鼠肝脏中的转录物也增加，注射胰岛素后其转录物减少。胰岛素介导的Insig-2a下降可能使SREBP-1c得以加工，从而即使在肝胆固醇水平升高的条件下，胰岛素也可以刺激脂肪酸合成。

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