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Biochem Biophys Res Commun. 1990 Sep 28;171(3):1244-51.

Monoclonal antibody alpha IR-3 inhibits the ability of insulin-like growth factor II to stimulate a signal from the type I receptor without inhibiting its binding.

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Department of Pharmacology, Stanford University School of Medicine, CA 94305.


We have previously shown that the protein encoded by a human insulin-like growth factor I (IGF-I) receptor cDNA binds both IGF-I and II with high affinity. In the present studies, we show that a monoclonal antibody to the IGF-I receptor, alpha IR-3, inhibits the binding of IGF-I but not IGF-II to the expressed receptor in intact cells and after solubilization. Surprisingly, this monoclonal antibody inhibits the ability of both IGF-I and II to stimulate thymidine synthesis in cells with the expressed receptor. Moreover, this antibody inhibits the ability of both IGF-I and II to stimulate the kinase activity of the IGF-I receptor in intact cells. These results indicate that alpha IR-3 binds to the IGF-I receptor in such a way that it does not inhibit the binding of IGF-II but does inhibit the subsequent ability of the receptor to be activated to transmit a signal.

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