...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Biochemistry >Insulin Silences Apolipoprotein B mRNA Translation by Inducing Intracellular Traffic into Cytoplasmic RNA Granules
【24h】

Insulin Silences Apolipoprotein B mRNA Translation by Inducing Intracellular Traffic into Cytoplasmic RNA Granules

机译：胰岛素通过诱导细胞内交通进入细胞质RNA颗粒沉默载脂蛋白B mRNA的翻译。

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

Insulin is a potent inducer of global mRNA translation and protein synthesis, yet it negatively regulates apolipoprotein B (apoB) mRNA translation, via an unknown mechanism. ApoB mRNA has a long half-life of 16 h, suggesting intracellular storage as mRNPs likely in the form of RNA granules. The availability of apoB mRNA for translation may be regulated by the rate of release from translationally silenced mRNPs within cytoplasmic foci called processing bodies (P bodies). In this report, we directly imaged intracellular apoB mRNA traffic and determined whether insulin silences apoB mRNA translation by entering cytoplasmic P bodies. We assessed the colocalization of apoB mRNA and β-globin mRNA (as a control) with P body (PB) markers using a strong interaction between the bacteriophage capsid protein MS2 and a sequence specific RNA stem–loop structure. We observed statistically significant increases in the localization of apoB mRNA into P bodies 4–16 h after insulin treatment (by 72–89%). The movement of apoB mRNA into cytoplasmic P bodies correlated with reduced translational efficiency as assessed by polysomal profiling and measurement of apoB mRNA abundance. PB localization of β-globin mRNA was insensitive to insulin treatment, suggesting selective regulation of apoB mRNA by insulin. Overall, our data suggest that insulin may specifically silence apoB mRNA translation by reprogramming its mRNA into P bodies and reducing the size of translationally competent mRNA pools. Translational control via traffic into cytoplasmic RNA granules may be an important mechanism for controlling the rate of apoB synthesis and hepatic lipoprotein production.
机译：胰岛素是整体mRNA翻译和蛋白质合成的有效诱导剂，但它通过未知机制对载脂蛋白B（apoB）mRNA的翻译负调控。 ApoB mRNA具有16小时的长半衰期，表明细胞内可能以RNA颗粒的形式作为mRNPs进行储存。 apoB mRNA用于翻译的可用性可能受称为加工体（P体）的细胞质灶内翻译沉默的mRNPs释放速率的调节。在此报告中，我们直接对细胞内apoB mRNA的流量进行成像，并确定胰岛素是否通过进入细胞质P体来沉默apoB mRNA的翻译。我们使用噬菌体衣壳蛋白MS2与序列特异性RNA茎-环结构之间的强相互作用，评估了apoB mRNA和β-珠蛋白mRNA与P体（PB）标记的共定位。我们观察到，在胰岛素治疗后4-16小时内，载脂蛋白B mRNA在P体中的定位有统计学意义的增加（增加了72-89％）。 apoB mRNA进入细胞质P体的运动与翻译效率的降低相关，如多体体谱分析和apoB mRNA丰度的测定所评估的。 PB对β-珠蛋白mRNA的定位对胰岛素治疗不敏感，提示胰岛素对apoB mRNA的选择性调节。总体而言，我们的数据表明，胰岛素可能通过将apoB mRNA重新编程为P体并减小翻译能力mRNA池的大小来特异性沉默apoB mRNA的翻译。通过运输进入细胞质RNA颗粒的翻译控制可能是控制载脂蛋白B合成和肝脂蛋白产生速率的重要机制。

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