title: Defective induction of stress-activated protein kinase activity in ataxia-telangiectasia cells exposed to ionizing radiation.
abstract: 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.
authors.affiliation: Joint Center for Radiation Therapy, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
authors.forename: T D
authors.initials: TD
authors.lastname: Shafman
authors.forename: A
authors.initials: A
authors.lastname: Saleem
authors.forename: J
authors.initials: J
authors.lastname: Kyriakis
authors.forename: R
authors.initials: R
authors.lastname: Weichselbaum
authors.forename: S
authors.initials: S
authors.lastname: Kharbanda
authors.forename: D W
authors.initials: DW
authors.lastname: Kufe
mesh_terms: D000841:Anisomycin / Q000494:pharmacology; D001260:Ataxia Telangiectasia / Q000201:enzymology*; D004789:Enzyme Activation / Q000187:drug effects / Q000528:radiation effects; D006801:Humans; D008214:Lymphocytes / Q000187:drug effects / Q000201:enzymology / Q000528:radiation effects; D011494:Protein Kinases / Q000378:metabolism / Q000528:radiation effects*; D013312:Stress, Physiological / Q000201:enzymology*; D013997:Time Factors
chemical_list: D000841:Anisomycin; D011494:Protein Kinases