GENERATION OF MOUSE MODELS OF NEUROLOGICAL DISORDERS

基因敲除小鼠模型已经成为描述 特定基因的分子和功能作用。 以试图 为神经系统疾病建立这样的模型，我们已经开始 破坏小鼠胚胎中载脂蛋白D（ApoD）基因的研究 干细胞我们用大鼠ApoD cDNA探针对129/svj小鼠进行了筛选， 基因组文库已经分离了八个ApoD基因组克隆， 表征了 ApoD靶向构建体已经被工程化用于 正/负选择 ApoD cDNA已通过RT-PCR从 小鼠肾脏RNA。 我们希望在实验室中产生ApoD基因敲除小鼠。 为了确定ApoD在神经再生中的作用， 以及它在乳腺癌和前列腺癌中的潜在作用。

Gene knock-out mouse models have become gold standards for delineating molecular and functional roles of specific genes. In an attempt to generate such models for neurological disorders, we have initiated studies to disrupt the apolipoprotein D (ApoD) gene in mouse embryonic stem cells. We have used rat ApoD cDNA probe to screen the 129/svj mouse genomic library. Eight genomic clones of ApoD have been isolated and characterized. An ApoD targeting construct has been engineered for positive/negative selection. ApoD cDNA has been cloned by RT-PCR from mouse kidney RNA. We expect to produce an ApoD knock-out mouse in the near future in order to determine the role of ApoD in nerve regeneration as well as its potential role in breast and prostate cancer.