Role of PRKCM (PKCmu) in radiation-induced increase of JUN proto-oncogene mRNA levels in B-lineage lymphoid cells.
Exposure of cells to ionizing radiation results in both activation of protein kinase C (PRKC, also known as PKC) and induction of transcription of the JUN proto-oncogene. PRKC plays a pivotal role in radiation-induced JUN expression, since inhibition of PRKC abrogates the JUN signal. However, the specific PRKC isoforms involved in radiation-induced elevation of JUN mRNA levels have not been identified. Here we demonstrate that in DT40 B-lineage lymphoid cells, the mu isoform of PRKC (PRKCM) is critical for the response of JUN to ionizing radiation. The zinc chelator, 1, 10-phenanthroline, abrogated induction of JUN after exposure to ionizing radiation, indicating that this PRKCM-mediated response is also dependent on zinc.
Department of Molecular Oncology, Parker Hughes Institute, St. Paul, Minnesota 55113, USA.
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D000818:Animals; D002614:Chelating Agents / Q000494:pharmacology; D002645:Chickens; D015342:DNA Probes; D004789:Enzyme Activation / Q000528:radiation effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005720:Gamma Rays; D005786:Gene Expression Regulation / Q000187:drug effects / Q000528:radiation effects; D016758:Genes, jun; D007527:Isoenzymes / Q000378:metabolism; D008223:Lymphoma; D018613:Microscopy, Confocal; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis*; D014158:Transcription, Genetic; D014407:Tumor Cells, Cultured; D015032:Zinc / Q000494:pharmacology
D002614:Chelating Agents; D015342:DNA Probes; D004791:Enzyme Inhibitors; D007527:Isoenzymes; D012333:RNA, Messenger; D011493:Protein Kinase C; D015032:Zinc