The gene expression in the kidney of selenium-binding protein1 deficient and C57BL/6J mice under 20 hours fasting condition. The gene expression in the kidney of selenium-binding protein1 deficient and C57BL/6J mice under 20 hours fasting condition

Selenium-binding protein 1 (Selenbp1) is a 2,3,7,8-tetrechlorodibenzo-p-dioxin inducible protein whose function is yet to be comprehensively elucidated. As the highly homologous isoform, Selenbp2, is expressed at low levels in the kidney, it is worthwhile to compare wild-type C57BL mice and Selenbp1-deficient mice under dioxin-free conditions. In this study, we conducted a comprehensive analysis of Selenbp1-Knockout mice to elucidate the role of Selenbp1 in the kidneys of wild-type C57BL mice under non-dioxin-administered conditions. Data from DNA microarray analysis suggested that Selenbp1 is involved in lipid metabolism. The results of real-time RT-PCR confirmed that ablation of Selenbp1 alters lipid metabolism via the Ppara pathway. Overall design: Total RNA were extracted from the kidney of wild-type and Selenbp1-KO mice at 8 weeks old under 20 hours fasting condition (each N=3) , and their cDNAs were applied to the analysis using Agilent -026655 Whole Mouse Genome Oligo DNA microarray (4X44K) version 2.

硒结合蛋白1（Selenbp1）是一种可被2,3,7,8-四氯二苯并对二噁英诱导的蛋白质，其功能尚未得到全面阐明。由于其高度同源的同工型Selenbp2在肾脏中低表达，因此在无二噁英条件下比较野生型C57BL小鼠与Selenbp1基因敲除小鼠具有重要研究价值。本研究对Selenbp1基因敲除小鼠开展全面分析，以阐明Selenbp1在未施加二噁英的条件下对野生型C57BL小鼠肾脏的作用。DNA微阵列分析数据显示，Selenbp1参与脂质代谢过程。实时荧光定量逆转录聚合酶链反应（real-time RT-PCR）结果证实，Selenbp1基因敲除可通过过氧化物酶体增殖物激活受体α（Ppara）通路改变脂质代谢。

实验整体设计：本研究从8周龄、经20小时禁食处理的野生型及Selenbp1基因敲除（Selenbp1-KO）小鼠肾脏中提取总RNA（每组样本量N=3），将其互补脱氧核糖核酸（cDNA）应用于安捷伦（Agilent）-026655全小鼠基因组寡核苷酸DNA微阵列（4×44K）版本2的分析。