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腺苷酸活化蛋白激酶(AMPK)与肝癌等肿瘤发生、发展有关。然而这方面的研究大都是基于体外细胞实验或小鼠移植瘤模型开展的。本文介绍一个运用白蛋白启动子驱动Cre(Alb-Cre)转基因,通过基因重组技术成功构建基因型为AMPKα1~(-/-)-Alb-Cre的转基因小鼠模型,肝脏特异表达的Cre重组酶在转基因小鼠中实现对肝脏AMPKα1特异性高效敲除。肝脏AMPKα1敲除后不影响小鼠的生长、繁殖及肝脏的结构。肝脏特异敲除AMPKα1小鼠模型的成功构建,为实现在动物整体水平对AMPK与肝脏代谢或肝癌的发生、发展的关系等方面的研究提供了基础。
Adenylate activated protein kinase (AMPK) and liver cancer and other related to the development. However, most researches in this area are based on in vitro cell experiments or mouse xenograft models. In this paper, a transgenic mouse model of AMPKα1 ~ (- / -) - Alb-Cre was successfully constructed by gene recombination using the albumin promoter-driven Cre (Alb-Cre) transgene, and liver-specific Cre recombinase Liver AMPKα1 is specifically and efficiently knocked out in transgenic mice. Liver AMPKα1 knockout does not affect mouse growth, reproduction and liver structure. The successful construction of the liver specific knockout AMPKα1 mouse model provides a basis for the study of the relationship between AMPK and hepatic metabolism or the occurrence and development of liver cancer in animal overall level.