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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.

No abstract