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Originally published In Press as doi:10.1074/jbc.M910045199 on March 23, 2000

J. Biol. Chem., Vol. 275, Issue 22, 16590-16596, June 2, 2000
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Amino-terminal-derived JNK Fragment Alters Expression and Activity of c-Jun, ATF2, and p53 and Increases H2O2-induced Cell Death*

Thomas Buschmann, Zhimin Yin, Anindita Bhoumik, and Ze'ev RonaiDagger

From the Ruttenberg Cancer Center, Mount Sinai School of Medicine, New York, New York 10029

The stress-activated protein kinase JNK plays an important role in the stability and activities of key regulatory proteins, including c-Jun, ATF2, and p53. To better understand mechanisms underlying the regulation of JNK activities, we studied the effect of expression of the amino-terminal JNK fragment (N-JNK; amino acids 1-206) on the stability and activities of JNK substrates under nonstressed growth conditions, as well as after exposure to hydrogen peroxide. Mouse fibroblasts that express N-JNK under tetracycline-off (tet-off) inducible promoter exhibited elevated expression of c-Jun, ATF2, and p53 upon tetracycline removal. This increased coincided with elevated transcriptional activities of p53, but not of c-Jun or ATF2, as reflected in luciferase activities of p21Waf1/Cip1-Luc, AP1-Luc, and Jun2-Luc, respectively. Expression of N-JNK in cells that were treated with H2O2 impaired transcriptional output as reflected in a delayed and lower level of c-Jun-, limited ATF2-, and reduced p53-transcriptional activities. N-JNK elicited an increase in H2O2-induced cell death, which is p53-dependent, because it was not seen in p53 null cells yet could be observed upon coexpression of p53 and N-JNK. The ability to alter the activity of ATF2, c-Jun, and p53 and the degree of stress-induced cell death by a JNK-derived fragment identifies new means to elucidate the nature of JNK regulation and to alter the cellular response to stress.

* Supported by National Institutes of Health Grants CA59008 and CA78419.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: Ruttenberg Cancer Center, Mount Sinai School of Medicine, 1425 Madison Ave. RM 15-20 New York, NY 10029. Tel.: 212-659-5571; Fax: 212-849-2446; E-mail: ronaiz01@doc.mssm.edu.

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