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The Journal of Immunology, 1998, 160: 3330-3336.
Copyright © 1998 by The American Association of Immunologists

Involvement of C-Abl Tyrosine Kinase in Lipopolysaccharide- Induced Macrophage Activation1

Quan Le, Rene Daniel, Siu-Wah Chung, Anthony D. Kang, Toby K. Eisenstein, Barnet M. Sultzer, Henry Simpkins and Peter M. C. Wong2

Fels Institute for Cancer Research and Molecular Biology, Departments of Pathology and Laboratory Medicine, Biochemistry, and Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140

LPS endotoxin-induced macrophage activation is recognized to be important in both nonspecific immunity and endotoxin-induced sepsis when excessive macrophage stimulation occurs. In this study, we showed that reduction of c-Abl in macrophages prevented LPS-induced growth arrest, nitric oxide production and TNF-{alpha} secretion by ANA-1 macrophages. These cells continued to grow but later underwent apoptosis. Reduction of c-Abl in these cells led to reduced c-Abl kinase activity associated with Ran, which recently has been shown to be an LPS-responsive gene product. Our data suggest that c-Abl tyrosine kinase is one of the intermediates downstream of the initial signal transduction event related to activation of macrophages by LPS.




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