首页> 外文期刊>BMC Neuroscience >Loss of IP3 receptor function in neuropeptide secreting neurons leads to obesity in adult Drosophila
【24h】

Loss of IP3 receptor function in neuropeptide secreting neurons leads to obesity in adult Drosophila

机译:分泌神经肽的神经元中IP3受体功能的丧失导致成人果蝇肥胖

获取原文
获取原文并翻译 | 示例
           

摘要

Background Intracellular calcium signaling regulates a variety of cellular and physiological processes. The inositol 1,4,5 trisphosphate receptor (IP3R) is a ligand gated calcium channel present on the membranes of endoplasmic reticular stores. In previous work we have shown that Drosophila mutants for the IP3R (itpr ku ) become unnaturally obese as adults with excessive storage of lipids on a normal diet. While the phenotype manifests in cells of the fat body, genetic studies suggest dysregulation of a neurohormonal axis.
机译:背景技术细胞内钙信号传导调节多种细胞和生理过程。肌醇1,4,5三磷酸受体(IP3R)是存在于内质网状存储膜上的配体门控钙通道。在以前的工作中,我们显示了IP3R的果蝇突变体(itpr ku),由于成年人在正常饮食中过多储存脂质而变得不自然肥胖。尽管表型表现在脂肪细胞中,但遗传研究表明神经激素轴失调。

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