首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Targeted inactivation of the insulin receptor gene in mouse 3T3-L1 fibroblasts via homologous recombination.
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Targeted inactivation of the insulin receptor gene in mouse 3T3-L1 fibroblasts via homologous recombination.

机译:通过同源重组使小鼠3T3-L1成纤维细胞中的胰岛素受体基因靶向失活。

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摘要

To study the role of the insulin receptor in determining adipocyte differentiation of the mouse cell line 3T3-L1, we have introduced a mutation that inactivates the insulin receptor gene by homologous recombination. In two independent clones, inactivation of one allele of the insulin receptor gene was associated with a 50-70% reduction in the number of insulin receptors. In addition, both clones were markedly impaired in their ability to differentiate into adipocytes. The defect in adipocyte-specific differentiation was corrected by expression of transfected human insulin receptor cDNA. These data suggest that the insulin receptor may play an important role in promoting differentiation of 3T3-L1 cells into adipocytes in vitro.
机译:为了研究胰岛素受体在确定小鼠细胞系3T3-​​L1的脂肪细胞分化中的作用,我们引入了通过同源重组使胰岛素受体基因失活的突变。在两个独立的克隆中,胰岛素受体基因的一个等位基因失活与胰岛素受体数量减少50-70%有关。此外,两个克隆的分化为脂肪细胞的能力均明显受损。通过转染的人胰岛素受体cDNA的表达纠正了脂肪细胞特异性分化的缺陷。这些数据表明胰岛素受体可能在体外促进3T3-L1细胞分化为脂肪细胞中起重要作用。

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