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Originally published In Press as doi:10.1074/jbc.M205413200 on October 11, 2002

J. Biol. Chem., Vol. 278, Issue 2, 1108-1114, January 10, 2003
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Erbin Suppresses the MAP Kinase Pathway*

Yang Z. HuangDagger , Mengwei Zang§, Wen C. Xiong, Zhijun Luo§, and Lin MeiDagger ||

From the Dagger  Departments of Neurobiology, Pathology, and Physical Medicine and Rehabilitation, Civitan International Research Center, University of Alabama at Birmingham, Birmingham, Alabama 35294-0021, the § Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, and the  Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0007

We present evidence here that Erbin is a negative regulator of the Ras-Raf-Erk signaling pathway. Expression of Erbin decreases transcription of the AChR epsilon -subunit gene, an event that is mediated by Erk activation. Although it interacts with the ErbB2 C terminus through the PDZ domain, Erbin has no effect on ErbB2 tyrosine phosphorylation or binding to the adaptor proteins Shc and Grb2. In contrast, expression of Erbin greatly impairs activation of Erk, but not Akt, by ligands that activate receptor tyrosine kinases. Moreover, Erbin inhibits the Erk activation by active Ras, while it fails to do so in the presence of active Raf-1. Erbin associates with active Ras, but not inactive Ras nor Raf. Consistently, Erbin interferes with the interaction between Ras and Raf both in vivo and in vitro. Finally, overexpression of Erbin leads to inhibition of NGF-induced neuronal differentiation of PC12 cells, whereas down-regulation of endogenous Erbin by specific siRNA exhibits an opposite effect. Collectively, our study has identified Erbin as a novel suppressor of the Ras signaling by disrupting the Ras-Raf interaction.

* This work was supported by National Institutes of Health Grant NS40480.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.

|| To whom correspondence should be addressed. E-mail: lmei@ nrc.uab.edu.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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