JBC Invitrogen Ultrasensitive Cytokine Assays

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Originally published In Press as doi:10.1074/jbc.C100050200 on February 23, 2001

J. Biol. Chem., Vol. 276, Issue 15, 11465-11468, April 13, 2001
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ACCELERATED PUBLICATION
The ARG Tyrosine Kinase Interacts with Siva-1 in the Apoptotic Response to Oxidative Stress*

Cheng Cao, Xinping Ren, Surender Kharbanda, Anthony KoleskeDagger , K. V. S. Prasad§, and Donald Kufe||

Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115 and Dagger  Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06520, and § Department of Microbiology and Immunology, University of Illinois at Chicago, Chicago, Illinois 60612

The Abl family of mammalian nonreceptor tyrosine kinases consists of c-Abl and ARG (Abl-related gene). Certain insights are available regarding the involvement c-Abl in the response of cells to stress. ARG, however, has no known function in cell signaling. The present studies demonstrate that ARG associates with the proapoptotic Siva-1 protein. The functional significance of the ARG-Siva-1 interaction is supported by the finding that ARG is activated by oxidative stress and that this response involves ARG-mediated phosphorylation of Siva-1 on Tyr48. The proapoptotic effects of Siva-1 are accentuated in cells stably expressing ARG and are inhibited in ARG-deficient cells. Moreover, the proapoptotic effects of Siva-1 are abrogated by mutation of the Tyr48 site. We also show that the apoptotic response to oxidative stress is attenuated in ARG-deficient cells and that this defect is corrected by reconstituting ARG expression. These findings support a model in which the activation of ARG by oxidative stress induces apoptosis by a Siva-1-dependent mechanism.

* This investigation was supported by Grant CA42802 awarded by the NCI, National Institutes of Health.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: Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney St., Boston, MA 02115. Tel.: 617-632-3141; Fax: 617-632-2934; E-mail: donald_kufe@dfci.harvard.edu.

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


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Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.