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Originally published In Press as doi:10.1074/jbc.M108033200 on January 7, 2002

J. Biol. Chem., Vol. 277, Issue 8, 6719-6725, February 22, 2002
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GIPC Participates in G Protein Signaling Downstream of Insulin-like Growth Factor 1 Receptor*

Ronald A. BoothDagger §, Cathy CummingsDagger , Mario TiberiDagger ||, and X. Johné LiuDagger §**Dagger Dagger

From the Dagger  Ottawa Health Research Institute, Ottawa Hospital, Ottawa K1Y 4E9, Canada and the Departments of § Biochemistry, Microbiology, and Immunology, || Cellular and Molecular Medicine, and ** Obstetrics and Gynaecology, University of Ottawa, Ottawa K1N 6N5, Canada

Several recent studies have demonstrated that insulin-like growth factor (IGF)-1-induced mitogen-activated protein kinase (MAP kinase) activation is abolished by pertussis toxin, suggesting that trimeric G proteins of the Gi class are novel cellular targets of the IGF-1 signaling pathway. We report here that the intracellular domain of the Xenopus IGF-1 receptor is capable of binding to the Xenopus homolog of mammalian GIPC, a PDZ domain-containing protein previously identified as a binding partner of Gi-specific GAP (RGS-GAIP). Binding of xGIPC to xIGF-1 receptor is independent of the kinase activity of the receptor and appears to require the PDZ domain of xGIPC. Injection of two C-terminal truncation mutants that retained the PDZ domain blocked IGF-1-induced Xenopus MAP kinase activation and oocyte maturation. While full-length xGIPC injection did not significantly alter insulin response, it greatly enhanced human RGS-GAIP in stimulating the insulin response in frog oocytes. This represents the first demonstration that GIPC·RGS-GAIP complex acts positively in IGF-1 receptor signal transduction.

* This work was supported by an operating grant from the Canadian Institute of Health Research (to X. J. L.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Recipient of an Ontario Graduate Scholarship in Science and Technology sponsored by the Ottawa Health Research Institute.

Dagger Dagger To whom correspondence should be addressed. Tel.: 613-798-5555 (ext. 17752); Fax: 613-761-5411 or 613-761-5365; E-mail: jliu@ohri.ca.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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