Targeted inactivation of the insulin receptor gene in mouse 3T3-L1 fibroblasts via homologous recombination.
AUTOR(ES)
Accili, D
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=51735Documentos Relacionados
- Antibody-induced Desensitization of the Insulin Receptor: STUDIES OF THE MECHANISM OF DESENSITIZATION IN 3T3-L1 FATTY FIBROBLASTS
- Interferon inhibits the conversion of 3T3-L1 mouse fibroblasts into adipocytes
- Interferon inhibits the conversion of 3T3-L1 mouse fibroblasts into adipocytes.
- Role of glycosylation and protein synthesis in insulin receptor metabolism by 3T3-L1 mouse adipocytes.
- Insulin receptor synthesis and turnover in differentiating 3T3-L1 preadipocytes.
