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Defective Induction of Stress-activated Protein Kinase Activity in Ataxia-Telangiectasia Cells Exposed to Ionizing Radiation¹

Joint Center for Radiation Therapy [T. D. S.] and Division of Cancer Pharmacology, Dana-Farber Cancer Institute [A. S., S. K., D. W. K.], Harvard Medical School, Boston, Massachusetts 02115; Diabetes Research Laboratories, Medical Services, Massachusetts General Hospital-East, Charlestown, Massachusetts 02114 [J. K.]; and Department of Radiation and Cellular Oncology, University of Chicago, Chicago, Illinois 60637 [R. W.]

The activity of stress-activated protein (SAP) kinase is stimulated by diverse agents such as tumor necrosis factor, UV light, and protein synthesis inhibitors. The present study demonstrates that ionizing radiation (IR) exposure is also associated with the induction of SAP kinase activity. Cells derived from patients with ataxia-telangiectasia (A-T) are characterized by hypersensitivity to IR. In this study, we demonstrate that IR-induced activation of SAP kinase is defective in A-T cells. In contrast, exposure of A-T cells to UV light or anisomycin results in the induction of SAP kinase activity. These findings indicate that IR-induced signals involved in SAP kinase activation are defective in A-T cells.

¹ This investigation was supported by USPHS Grant CA55241 awarded by the National Cancer Institute, Department of Health and Human Services.

² To whom requests for reprints should be addressed, at Joint Center for Radiation Therapy/SWRL, 50 Binney Street, Boston, MA 02115.

Received 5/ 3/95. Accepted 6/16/95.

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