![]()
|
|
||||||||
J. Biol. Chem., Vol. 278, Issue 32, 29667-29675, August 8, 2003
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||


¶
From the
Dana-Farber Cancer Institute, Harvard
Medical School, Boston, Massachusetts 02115 and the
Beijing Institute of Biotechnology, Beijing
100850, People's Republic of China
The Abl family of mammalian non-receptor tyrosine kinases includes c-Abl and Arg. Recent studies have demonstrated that c-Abl and Arg are activated in the response of cells to oxidative stress. This work demonstrates that catalase, a major effector of the cellular defense against H2O2, interacts with c-Abl and Arg. The results show that H2O2 induced binding of c-Abl and Arg to catalase. The SH3 domains of c-Abl and Arg bound directly to catalase at a P293FNP site. c-Abl and Arg phosphorylated catalase at Tyr231 and Tyr386 in vitro and in the response of cells to H2O2. The functional significance of the interaction is supported by the demonstration that cells deficient in both c-Abl and Arg exhibit substantial increases in H2O2 levels. In addition, c-abl/ arg/ cells exhibited a marked increase in H2O2-induced apoptosis compared with that found in the absence of either kinase. These findings indicate that c-Abl and Arg regulate catalase and that this signaling pathway is of importance to apoptosis in the oxidative stress response.
Received for publication, February 5, 2003 , and in revised form, May 29, 2003.
* This work was supported by NCI Grants CA42802 and CA49639 from the National Institutes of Health. The costs of publication of this article were defrayed in part by the payment of page charges. This 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., Harvard Medical School, Boston, MA 02115. Tel.: 617-632-3141; Fax: 617-632-2934; E-mail: donald_kufe{at}dfci.harvard.edu.
![]()
CiteULike
Complore
Connotea
Del.icio.us
Digg
Reddit
Technorati What's this?
This article has been cited by other articles:
![]() |
S. Z. Imam, F. E. Indig, W.-H. Cheng, S. P. Saxena, T. Stevnsner, D. Kufe, and V. A. Bohr Cockayne syndrome protein B interacts with and is phosphorylated by c-Abl tyrosine kinase Nucleic Acids Res., August 1, 2007; 35(15): 4941 - 4951. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. G. Menon, E. H. Sarsour, A. L. Kalen, S. Venkataraman, M. J. Hitchler, F. E. Domann, L. W. Oberley, and P. C. Goswami Superoxide Signaling Mediates N-acetyl-L-cysteine-Induced G1 Arrest: Regulatory Role of Cyclin D1 and Manganese Superoxide Dismutase Cancer Res., July 1, 2007; 67(13): 6392 - 6399. [Abstract] [Full Text] [PDF] |
||||
![]() |
Z.-L. Xiao, J. Amaral, P. Biancani, and J. Behar Impaired cytoprotective function of muscle in human gallbladders with cholesterol stones Am J Physiol Gastrointest Liver Physiol, March 1, 2005; 288(3): G525 - G532. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. He, Y. Tohyama, K.-i. Yamamoto, M. Kobayashi, Y. Shi, T. Takano, C. Noda, K. Tohyama, and H. Yamamura Lysosome is a primary organelle in B cell receptor-mediated apoptosis: an indispensable role of Syk in lysosomal function Genes Cells, January 1, 2005; 10(1): 23 - 35. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Fukamatsu, N. Yabe, and K. Hasunuma Arabidopsis NDK1 is a Component of ROS Signaling by Interacting with Three Catalases Plant Cell Physiol., October 15, 2003; 44(10): 982 - 989. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Cao, Y. Leng, W. Huang, X. Liu, and D. Kufe Glutathione Peroxidase 1 Is Regulated by the c-Abl and Arg Tyrosine Kinases J. Biol. Chem., October 10, 2003; 278(41): 39609 - 39614. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |