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J. Biol. Chem., Vol. 279, Issue 7, 5837-5845, February 13, 2004

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H₂O₂-dependent Activation of GCLC-ARE4 Reporter Occurs by Mitogen-activated Protein Kinase Pathways without Oxidation of Cellular Glutathione or Thioredoxin-1^*

Young-Mi Go, Jerry J. Gipp, R. Timothy Mulcahy¶, and Dean P. Jones||**

From the Department of Medicine, Division of Cardiology, School of Medicine, ^||Center for Clinical and Molecular Nutrition, Emory University, Atlanta, Georgia 30322 and the Department of Surgery and ^¶Pharmacology, University of Wisconsin Medical School, Madison, Wisconsin 53792

The gp91^phox homologue Nox1 produces H₂O₂, which induces cell growth, transformation, and tumorigenicity. However, it has not been clear whether H₂O₂ effects are mediated indirectly via a generally oxidizing cellular environment or whether H₂O₂ more directly targets specific signaling pathways. Here, we investigated signaling by H₂O₂ induced by Nox1 overexpression using a luciferase reporter regulated by the antioxidant response element ARE4. Surprisingly, Nox1-derived H₂O₂ activated the reporter gene 15-fold with no effect on the redox state of the major thiol antioxidant substances, glutathione and thioredoxin. H₂O₂ signaling to ARE4 was mediated by activation of both the c-Jun N-terminal kinase and ERK1/2 pathways modulated by Ras. Thus, "redox signaling" resulting in kinase signaling pathways is distinct from "oxidative stress," and is mediated by discrete, localized redox circuitry.

Received for publication, July 14, 2003 , and in revised form, October 6, 2003.

^* This work was supported by National Institutes of Health Grant ES011195. The costs of publication of this article were defrayed in part by the payment of page charges. This 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: Dept. of Medicine, 4131 Rollins Research Center, Emory University, Atlanta, GA 30322. Tel.: 404-727-5970; Fax: 404-727-3231; E-mail: dpjones{at}emory.edu.

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