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A functional insulin-like growth factor I receptor is required for the mitogenic and transforming activities of the epidermal growth factor receptor.
Author(s) -
Domenico Coppola,
Andres Ferbér,
Masahiko Miura,
Christian Sell,
Consuelo D'Ambrosio,
Raphael Rubin,
Renato Baserga
Publication year - 1994
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.14.7.4588
Subject(s) - biology , epidermal growth factor , insulin like growth factor 1 receptor , transfection , growth factor , epidermal growth factor receptor , receptor , growth factor receptor , fibroblast growth factor receptor 4 , microbiology and biotechnology , growth factor receptor inhibitor , fibroblast growth factor receptor 3 , transforming growth factor , transforming growth factor, beta 3 , tgf alpha , fibroblast growth factor , cell culture , signal transduction , fibroblast growth factor receptor , genetics
When wild-type mouse embryo cells are stably transfected with a plasmid constitutively overexpressing the epidermal growth factor (EGF) receptor (EGFR), the resulting cells can grow in serum-free medium supplemented solely with EGF. Supplementation with EGF also induces in these cells the transformed phenotype (growth in soft agar). However, when the same EGFR expression plasmid is introduced and overexpressed in cells derived from littermate embryos in which the insulin-like growth factor I (IGF-I) receptor genes have been disrupted by homologous recombination, the resulting cells are unable to grow or to be transformed by the addition of EGF. Reintroduction into these cells (null for the IGF-I receptor) of a wild-type (but not of a mutant) IGF-I receptor restores EGF-mediated growth and transformation. Our results indicate that at least in mouse embryo fibroblasts, the EGFR requires the presence of a functional IGF-I receptor for its mitogenic and transforming activities.

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