...
首页> 外文期刊>Lipids >INCREASED HEPATIC SYNTHESIS AND ACCUMULATION OF PLASMA APOLIPOPROTEIN B100 IN COPPER-DEFICIENT RATS DOES NOT RESULT FROM MODIFICATION IN APOLIPOPROTEIN B MRNA EDITING
【24h】

INCREASED HEPATIC SYNTHESIS AND ACCUMULATION OF PLASMA APOLIPOPROTEIN B100 IN COPPER-DEFICIENT RATS DOES NOT RESULT FROM MODIFICATION IN APOLIPOPROTEIN B MRNA EDITING

机译:缺铜大鼠血浆中载脂蛋白B100肝合成和积累的增加并非源自载脂蛋白B MRNA编辑的修饰

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

Experimentally induced copper deficiency in the rat results in increased plasma apolipoprotein B100 (ape B100) concentration in association with increased hepatic apo B100 synthesis. This enhancement of apo B100 synthesis and plasma accumulation accounts for the rise of plasma low density lipoprotein in these animals. In the present study, we have investigated if the selective increase in hepatic apo B100 synthesis is accounted for by changes in apo B mRNA editing. Reverse transcription coupled with polymerase chain reaction amplification and primer extension analysis of apo B cDNA revealed no differences in apo B mRNA editing in either the liver or small intestine between control and copper-deficient rats. We speculate that the increase in apo B100 synthesis in the liver of copper-deficient rats reflects posttranslational alterations in gene expression accompanying changes in very low density lipoprotein assembly and secretion. [References: 22]
机译:实验中诱导的大鼠铜缺乏导致血浆载脂蛋白B100(猿B100)浓度增加,同时肝脏载脂蛋白B100合成增加。 Apo B100合成和血浆积聚的这种增强解释了这些动物中血浆低密度脂蛋白的升高。在本研究中,我们已经研究了肝载脂蛋白B100合成的选择性增加是否是由载脂蛋白B mRNA编辑的改变引起的。逆转录结合聚合酶链反应扩增和载脂蛋白B cDNA的引物延伸分析显示,对照组和缺铜大鼠在肝脏或小肠中载脂蛋白B mRNA编辑无差异。我们推测缺铜大鼠肝脏中载脂蛋白B100合成的增加反映了伴随极低密度脂蛋白装配和分泌变化的基因表达的翻译后改变。 [参考:22]

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