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Originally published In Press as doi:10.1074/jbc.M101414200 on February 28, 2001

J. Biol. Chem., Vol. 276, Issue 20, 17281-17285, May 18, 2001
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Targeting of the c-Abl Tyrosine Kinase to Mitochondria in the Necrotic Cell Death Response to Oxidative Stress*

Shailendra KumarDagger , Ajit BhartiDagger , Neerad C. Mishra§, Deepak RainaDagger , Surender KharbandaDagger , Satya Saxena§, and Donald KufeDagger

From the Dagger  Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115 and the § Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87115

The ubiquitously expressed c-Abl tyrosine kinase is activated in the response of cells to genotoxic and oxidative stress. The present study demonstrates that reactive oxygen species (ROS) induce targeting of c-Abl to mitochondria. We show that ROS-induced localization of c-Abl to mitochondria is dependent on activation of protein kinase C (PKC)delta and the c-Abl kinase function. Targeting of c-Abl to mitochondria is associated with ROS-induced loss of mitochondrial transmembrane potential. The results also demonstrate that c-Abl is necessary for ROS-induced depletion of ATP and the activation of a necrosis-like cell death. These findings indicate that the c-Abl kinase targets to mitochondria in response to oxidative stress and thereby mediates mitochondrial dysfunction and cell death.

* This work was supported by Grant CA42802 awarded by the NCI, National Institutes of Health, the Department of Health and Human Services, and by the office of Health and Biological Research, United States Department of Energy cooperative agreement DE-FC04-96AL76406.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 Inst., 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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