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Originally published In Press as doi:10.1074/jbc.M002490200 on August 31, 2000

J. Biol. Chem., Vol. 275, Issue 46, 35920-35925, November 17, 2000
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Basic Fibroblast Growth Factor Utilizes Both Types of Component Subunits of Gs for Dual Signaling in Human Adipocytes
STIMULATION OF ADENYLYL CYCLASE VIA Galpha s AND INHIBITION OF NADPH OXIDASE BY Gbeta gamma s*

Heidemarie I. Krieger-BrauerDagger , Pankaj Medda, and Horst Kather

From the Klinisches Institut für Herzinfarktforschung an der Medizinischen Universitätsklinik, Bergheimerstraße 58, D-69115 Heidelberg, Germany

Basic fibroblast growth factor (bFGF), a ligand of receptor protein-tyrosine kinases, promoted the dissociation of Gs and had antagonistic stimulatory and inhibitory effects on adenylyl cyclase and NADPH oxidase in human fat cell plasma membranes. The bFGF-induced activation of adenylyl cyclase was blocked by COOH-terminal anti-Galpha s, indicating that it was mediated by Galpha s. The inhibitory action of bFGF was mimicked by exogenously supplied Gbeta gamma -subunits and was reversed by anti-Gbeta 1/2, or beta ARK-CT, a COOH-terminal beta -adrenergic receptor kinase fragment that specifically binds free Gbeta gamma , indicating that it was transduced by Gbeta gamma complexes. The bFGF-induced inhibition of NADPH-dependent H2O2 generation was also reversed by peptide 100-119, an inhibitor of Gs activation by ligand-occupied beta -adrenergic receptors, indicating that the Gbeta gamma complexes mediating the inhibitory action of the growth factor are derived from Gs. The findings suggest a direct, non-kinase-dependent, coupling of bFGF receptor(s) to Gs and provide the first example of a ligand of receptor protein-tyrosine kinases that is capable of utilizing both types of component subunits of a single heterotrimeric G protein for dual signaling in a single cell type.

* This work was supported by a grant from the Deutsche Forschungsgemeinschaft, Bonn-Bad Godesberg, Germany.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.

Dagger To whom correspondence should be addressed. Tel.: 49-6221-568775; Fax: 49-6221-565342; E-mail: horst_kather@med.uni- heidelberg.de.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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