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Originally published In Press as doi:10.1074/jbc.M201717200 on April 26, 2002

J. Biol. Chem., Vol. 277, Issue 27, 24197-24203, July 5, 2002
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Bi-directional Regulation of UV-induced Activation of p38 Kinase and c-Jun N-terminal Kinase by G Protein beta gamma -Subunits*

MiRan SeoDagger , Yun-Il LeeDagger , Chin-Ho ChoDagger , Chang-Dae Bae§, In-Hoo Kim, and Yong-Sung JuhnnDagger ||

From the Dagger  Department of Biochemistry and Cancer Research Institute, Seoul National University College of Medicine, Seoul 110-799, Korea, the § Department of Biochemistry and Molecular Biology, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea, and the  Division of Basic Science, National Cancer Center, Koyang 411-764, Korea

Ultraviolet (UV) irradiation induces various cellular responses by activating many UV-responsive enzymes including mitogen-activated protein kinases (MAPKs). Various G protein-coupled receptor agonists also activate MAPKs, but it is not known whether or not G proteins also mediate the UV-induced activation of MAPKs. Therefore, this study was undertaken to determine whether the G protein beta gamma -subunit (Gbeta gamma ) mediates the UV-induced activation of p38 and JNK. Gbeta gamma overexpression in COS-1 cells amplified the UV-induced activation of p38 but reduced JNK activation. The overexpression of the C-terminal region of beta -adrenergic receptor kinase (beta ARKct) decreased the UV-induced activation of p38 but increased JNK activation. Gbeta 1gamma 2 expression increased MKK3/6 phosphorylation with a concomitant decrease in MKK4 phosphorylation, which contrasts with beta ARKct expression. Gbeta 1gamma 2 or beta ARKct expression resulted in corresponding changes in the transcriptional activity of CHOP and c-Jun. Treatment with a p38 inhibitor, SB203580, or the expression of a kinase-inactive p38 increased the UV-induced JNK activation. Expression of the constitutively active MKK6 decreased the UV-induced JNK activation. In summary, although the endogenous Gbeta gamma was found to mediate about half of the UV-induced activation of p38, it was found that exogenous Gbeta gamma mediates the bi-directional regulation of UV-induced p38 and JNK activation, and that this bi-directional regulation results from the inhibition of JNK activation by the p38 activated via Gbeta gamma in the COS-1 cells.

* This study was supported by the NONDIRECT RESEARCH FUND, Korea Research Foundation (1996) and by the academic research fund of the Ministry of Education, Republic of Korea Research foundation (1997). This study was also supported in part by the 2002 BK21 project for Medicine, Dentistry, and Pharmacy and by a research grant from the Cancer Research Institute, Seoul National University College of Medicine (2001).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: Dept. of Biochemistry and Molecular Biology, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul 110-799, Korea. Tel.: 82-2-740-8247; Fax: 82-2-744-4534; E-mail: juhnn@snu.ac.kr.

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