肝脏特异敲除腺苷酸活化蛋白激酶小鼠模型的建立

Establishment of a mice model with liver-specific AMP-activated protein kinase gene knockout

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。

AMP-activated protein kinase （AMPK） is involved in the development and progression of tumors including hepatocellular carcinoma （HCC）. However, studies on AMPK and tumorigenesis were largely based on experiments in vitro or tumor xenografts model. Here, we introduce a liver-specific AMPKal knockout mice model, which is achieved by Alb-Cre recombinase system. The expression of AMPKul in the liver of AMPKα1^-/--Alb-Cre mice is absent. AMPKal knockout in the liver does not affect the growth and histological structure of mouse liver. This model provides a favorable tool to the study of the roles of AMPKα1 in liver metabolism or tumorigenesis.