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Originally published In Press as doi:10.1074/jbc.M004615200 on January 31, 2001

J. Biol. Chem., Vol. 276, Issue 18, 14572-14580, May 4, 2001
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UVA Induces Ser381 Phosphorylation of p90RSK/MAPKAP-K1 via ERK and JNK Pathways*

Yiguo ZhangDagger , Shuping Zhong, Ziming Dong§, Nanyue ChenDagger , Ann M. BodeDagger , Wei-ya MaDagger , and Zigang DongDagger

From Dagger  The Hormel Institute, University of Minnesota, Austin, Minnesota 55912 and the § Department of Pathophysiology, Henan Medical University, Zhengzhou 450052, Peoples Republic of China

UVA exposure plays an important role in the etiology of skin cancer. The family of p90-kDa ribosomal S6 kinases (p90RSK/MAPKAP-K1) are activated via phosphorylation. In this study, results show that UVA-induced phosphorylation of p90RSK at Ser381 through ERKs and JNKs, but not p38 kinase pathways. We provide evidence that UVA-induced p90RSK phosphorylation and kinase activity were time- and dose-dependent. Both PD98059 and a dominant negative mutant of ERK2 blocked ERKs and p90RSK Ser381 phosphorylation, as well as p90RSK activity. A dominant negative mutant of p38 kinase blocked UVA-induced phosphorylation of p38 kinase, but had no effect on UVA-induced Ser381 phosphorylation of p90RSK or kinase activity. UVA-induced p90RSK phosphorylation and kinase activity were markedly attenuated in JnK1-/- and JnK2-/- cells. A dominant negative mutant of JNK1 inhibited UVA-induced JNKs and p90RSK phosphorylation and kinase activity, but had no effect on ERKs phosphorylation. PD169316, a novel inhibitor of JNKs and p38 kinase, inhibited phosphorylation of p90RSK, JNKs, and p38 kinase, but not ERKs. However, SB202190, a selective inhibitor of p38 kinase, had no effect on p90RSK or JNKs phosphorylation. Significantly, ERKs and JNKs, but not p38 kinase, immunoprecipitated with p90RSK when stimulated by UVA and p90RSK was a substrate for ERK2 and JNK2, but not p38 kinase. These data indicate clearly that p90RSK Ser381 may be phosphorylated by activation of JNKs or ERKs, but not p38 kinase.

* This work was supported by The Hormel Foundation and National Institutes of Health Grants CA77646 and CA81064.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. Tel.: 507-437-9640; Fax: 507-437-9606; E-mail: zgdong@smig.net.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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