Abstract
53BP1 is rapidly recruited at sites of DNA double-strand breaks (DSBs) after treatment of cells with ionizing radiation, and is suggested to be involved in DNA damage checkpoint and non-homologous end-joining (NHEJ) repair of DNA DSBs. Recently, some of the NHEJ repair proteins has been reported to play a regulatory role in apoptosis. However, it is still unclear whether or not 53BP1 is involved in apoptosis. To investigate a role of 53BP1 in apoptosis, we examined expression of 53BP1 in apoptotic cells. T cell leukemia cell line Jurkat, cells were treated with an apoptosis-inducing agent, staurosporine, and cell extracts harvested every 2 hours after exposure of staurosporine were subjected to immunoblotting analysis. We found that 53BP1 was reduced after induction of apoptosis in cells. Furthermore, we found that expression of some of the NHEJ proteins, such as Ku70, Ku80 and XRCC4, is reduced in apoptotic cells. In contrast, DNA-PKcs expression was elevated after apoptosis induction. We would like to discuss a potential role of 53BP1 in apoptotic cells.
