Open AccessTargeted inactivation of the insulin receptor gene in mouse 3T3-L1 fibroblasts via homologous recombination.
Author(s) -
Domenico Accili,
Simeon I. Taylor
Publication year - 1991
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.88.11.4708
Subject(s) - insulin receptor , biology , receptor , homologous recombination , adipocyte , transfection , microbiology and biotechnology , insulin like growth factor 1 receptor , insulin , insulin receptor substrate , 3t3 l1 , irs2 , gene , adipose tissue , genetics , endocrinology , insulin resistance , growth factor
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.