阿尔茨海默氏病（Alzheimer's disease,AD）是一种发生在老年期及老年前期的原发性退行性脑病。现有的研究结果表明人脑中钙调磷酸酶（calcineurin，CN)的活力的降低很可能是阿尔茨海默氏病发生的重要原因。RCAN1基因（regulators of calcineurin I gene）是CN的重要内源性调节基因。近几年的研究发现，RCAN1基因在AD病人脑中发生了过量表达。因此，研究RCAN1基因在细胞内的过表达情况以及体外RCAN1蛋白与CN间的相互作用具有十分现实的意义。 本研究分别从人源神经母细胞瘤SY5Y及鼠脑组织中克隆出RCAN1-1L基因，选择合适的质粒载体，构建出RCAN1-1L基因的原核和真核表达质粒。结果表明，SY5Y神经瘤细胞中的RCAN1-1L基因已经发生突变，无法获得正确的目的基因。本实验从鼠脑组织中成功克隆出了RCAN1-1L基因，获得了RCAN1-1L的真核和原核表达质粒，为研究RCAN1-1L基因在细胞内的过表达情况以及体外RCAN1-1L蛋白与CN间的相互作用提供了一定的实验基础。

Alzheimer's disease (AD), the most common cause of cognitive disturbance and dementia, is a progressive neurodegenerative disease. Studies have found that the decline in calcineurin(CN) activity may have an important role in the development of AD. RCAN1 is an important endogenous regulating gene of CN，which is found to be overexpressed in neurons from Alzheimer’s disease patients. Thereofore, it is really significant to do research about the overexpression of RCAN1 in cells and the interaction between RCAN1 and CN. This experiment aimed at constructing prokaryotic and eukaryotic expression plasmids. METHODS: hRCAN1-1L and mRCAN1-1L genes were cloned from SY5Y cell and mouse brain by using RT-PCR method. Recombinant clones were selected by blue white plaque assay and PCR Screen after target gene were subcloned into pEASY- T1 Cloning Vector. Sequencing assays showed that the sequence of hRCAN1-1L cloned from SY5Y cell was not correct, therefore we constructed eukaryotic mRCAN11-1L-pEGFP-N2 plasmid and prokaryotic mRCAN11-1L-pGEX-4T-1 plasmid by using restriction enzymes. This might lay foundation for the study of the overexpression of RCAN1 in cells and the interaction between RCAN1 and CN.