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通过同源重组对小鼠3T3-L1成纤维细胞中的胰岛素受体基因进行靶向失活。

Targeted inactivation of the insulin receptor gene in mouse 3T3-L1 fibroblasts via homologous recombination.

作者信息

Accili D, Taylor S I

机构信息

Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892.

出版信息

Proc Natl Acad Sci U S A. 1991 Jun 1;88(11):4708-12. doi: 10.1073/pnas.88.11.4708.

DOI:10.1073/pnas.88.11.4708
PMID:2052553
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC51735/
Abstract

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.

摘要

为了研究胰岛素受体在决定小鼠细胞系3T3-L1脂肪细胞分化中的作用,我们通过同源重组引入了一个使胰岛素受体基因失活的突变。在两个独立的克隆中,胰岛素受体基因一个等位基因的失活与胰岛素受体数量减少50 - 70%相关。此外,两个克隆在分化为脂肪细胞的能力上均明显受损。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细胞向脂肪细胞分化中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/a65e75a07b65/pnas01061-0157-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/b8d036fc49e2/pnas01061-0155-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/10dcb209abe0/pnas01061-0155-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/37ba84a15edd/pnas01061-0155-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/8f784d349990/pnas01061-0155-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/92fb60f5337a/pnas01061-0155-e.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/469afec3b59c/pnas01061-0155-f.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/4bcd05da9913/pnas01061-0156-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/7769943e85b4/pnas01061-0156-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/ac0c87b53662/pnas01061-0157-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/a65e75a07b65/pnas01061-0157-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/b8d036fc49e2/pnas01061-0155-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/10dcb209abe0/pnas01061-0155-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/37ba84a15edd/pnas01061-0155-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/8f784d349990/pnas01061-0155-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/92fb60f5337a/pnas01061-0155-e.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/469afec3b59c/pnas01061-0155-f.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/4bcd05da9913/pnas01061-0156-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/7769943e85b4/pnas01061-0156-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/ac0c87b53662/pnas01061-0157-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c188/51735/a65e75a07b65/pnas01061-0157-b.jpg

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