中文摘要：

目的：构建FKBP38（FK506 Binding Protein 38）基因肝脏特异敲除小鼠。方法：利用胚胎注射法构建在FKBP38上携带lox P位点的转基因小鼠。在FKBP38基因位置携带lox P位点的小鼠的基础上,以肝脏实质细胞特异性表达的Alb-Cre介导FKBP38条件性敲除,以获得FKBP38基因肝脏特异敲除小鼠模型Alb-Cre：FKBP38^fl/fl。同时对FKBP38特异性敲除鼠进行鉴定。结果：①FKBP38肝脏特异敲除小鼠FKBP38^-/-肝脏中FKBP38基因的m RNA水平相对于同年龄同窝野生型小鼠具有统计学差异（P〈0.001）。②FKBP38肝脏特异敲除小鼠FKBP38^-/-肝脏中FKBP38基因的蛋白表达水平相对于同年龄同窝野生型小鼠具有统计学差异（P〈0.001）。③FKBP38肝脏特异敲除小鼠FKBP38^-/-肝脏中,转录和翻译相关蛋白水平未见显著差异,p70 S6K的磷酸化水平轻微上调,4EBP-1的磷酸化水平有轻微下调。（4）FKBP38肝脏特异敲除小鼠FKBP38^-/-肝脏中,凋亡相关蛋白Bcl-2未见差异化表达。结论：FKBP38肝脏特异敲除小鼠FKBP38^-/-肝脏中,FKBP38基因的m RNA和蛋白基本不表达,提示成功构建FKBP38基因肝脏特异敲除小鼠。

英文摘要：

Objective： To build the model of the gene FKBP38 （FK506 binding protein 38） conditional knock out in liver. Methods： Transgenic mouse whose FKBP38 gene was flanked with loxP was constructed by embryo microinjection. The FKBP38 gene was deleted by breeding mice harboring two loxP sites in FKBP38 （FKBP38^fl/fl） with the mice bearing the expression ofCre recombinase mice driven by an album promoter. Afterward, the genotype of FKBP38 conditional knockout mice was analyzed. Results： （1）Relative hepatic FKBP38 mRNA levels showed significant difference between FKBP38 conditional knockout mice （FKBP38^-/-） and wild type（P〈 0.001）. （2）Relative hepatic FKBP38 protein expression levels of FKBP38 conditional knockout mice （FKBP38^-/-） were significantly different with wild type（P〈0.001）.（3）Relative phosphorylation of hepatic p70 S6K and 4E-BP-1 protein of FKBP38 conditional knockout mice （FKBP38^-/-） showed no significant difference, with slight decrease in phosphorylation of 4E-BP-1, compared with wild type. （4）No significant difference in expression of hepatic Bcl-2 between FKBP38^-/- and wild type. Conclusions： The mouse model of the gene FKBP38 （FK506 binding protein 38） conditional knock out in liver is successfully built.