Control mechanism of radiation-induced apoptosis and function of protein kinase C

In this review, the cellular radiation response is discussed from an aspect of control of apoptosis related to protein kinase C (PKC) cascades and their network. It has been recognized that PKC is a membrane-dependent enzyme(s), radiation activates PKC and modification of PKC activity alters the cellular radiation sensitivity. Radiation induces cell responses either for or against apoptosis dependent on isoforms of PKC. PKCα suppresses apoptosis induced by radiation. PKCδ acts as an apoptotic signal through ATM/c-Abl cascade in cell nucleus or in downstream of p53 pathway in mitochondria: the function of the PKCδ is quite complicated dependently on its intracellular location and types of the cell and tissue. Cross-talks between PKC and ATM have been recently reported to be important toward or outward apoptosis. The current focus of author's research is to identify the regulatory molecule(s) of PKCδ that which determine the radiation sensitivity. (T.I.)