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Role of Tyrosine Phosphorylation in Radiation-induced Activation of c-jun Protooncogene in Human Lymphohematopoietic Precursor Cells¹

Section of Cancer and Leukemia Biology, Departments of Therapeutic Radiology-Radiation Oncology, Pharmacology, Pediatrics, and the Bone Marrow Transplantation Program, University of Minnesota, Minneapolis, Minnesota 55455

We examined the effects of ionizing radiation on c-jun expression in human lymphohematopoietic precursors. Radiation exposure increased the level of c-jun transcripts in a dose- and time-dependent manner, providing direct evidence that ionizing radiation can activate c-jun protooncogene in human lymphohematopoietic precursors. Notable -rays failed to induce c-jun expression in cells pretreated with herbimycin, and the use of cycloheximide did not overcome the inhibitory effects of herbimycin. The lack of c-jun signal in herbimycin-treated cells was not due to nonspecific damage to the distal protein kinase C signaling pathway. Thus, protein tyrosine kinase activation precedes and perhaps mandates radiation-induced activation of c-jun protooncogene expression in human lymphohematopoietic precursors.

¹ This work was supported by USPHS Grant R29 CA 42111. F. M. U. is a Scholar of the Leukemia Society of America. This is Publication 85 from the Tumor Immunology Laboratory, University of Minnesota. This work is part of a doctoral thesis by H. P. C. to fulfill the requirements of the University of Minnesota Graduate School.

² To whom requests for reprints should be addressed, at Box 356 UMHC, Section of Cancer and Leukemia Biology, Dept. of Therapeutic Radiology, University of Minnesota, 420 Delaware Street S.E., Minneapolis, MN 55455.

Received 7/16/92. Accepted 12/15/92.

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