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Volume 271, Number 38, Issue of September 20, 1996 pp. 23304-23309
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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Activation of c-Jun-NH₂-Kinase by UV Irradiation Is Dependent on p21^ras

(Received for publication, April 22, 1996, and in revised form, June 26, 1996)

Victor Adler ^§ , Matthew R. Pincus ^§ , Alla Polotskaya , Ximena Montano ^¶ , Fred K. Friedman and Ze'ev Ronai

From the  Molecular Carcinogenesis Program, American Health Foundation, Valhalla, New York 10595, ^§ Department of Pathology and Laboratory Medicine, Veterans Affairs Medical Center, Brooklyn, New York 11209 and SUNY Health Science Center, Brooklyn, New York 11203, ^¶ Imperial Cancer Research Fund, 44 Lincoln's Inn Fields, London, United Kingdom, and  Laboratory of Molecular Carcinogenesis, NCI, National Institutes of Health, Bethesda, Maryland 20892

We have demonstrated previously that Jun-NH₂-kinase (JNK) activation in vitro is potentiated by association with the p21^ras protein. To determine if in vivo activation of JNK also depends on p21^ras, we have used M1311 cells that carry the cDNA for the neutralizing antibody to p21^ras, Y13-259, under a dexamethasone-inducible promoter. The ability of UV to activate JNK gradually decreased over a 4-day period of cell growth in dexamethasone. This decrease coincides with weaker transcriptional activation measured via gel shift and chloramphenicol acetyltransferase assays. Peptides corresponding to amino acids 96-110 on p21^ras, which were shown to block Ras-JNK association, inhibited UV-mediated JNK activation in mouse fibroblast 3T3-4A cells as well as in M1311 cells, further supporting the role of p21^ras in UV-mediated JNK activation. Overall, the present studies provide in vivo confirmation of the role p21^ras plays in JNK activation by UV irradiation.

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