Affiliation: | aCenter for Childhood Cancer, Children's Research Institute, The Ohio State University, College of Medicine and Public Health, 700 Children's Drive, Columbus, OH 43205-2696, United States bDivision of Neurology, Children's Hospital, The Ohio State University, 700 Children's Drive, Columbus, OH 43205-2696, United States cDepartment of Pediatrics, The Ohio State University, 700 Children's Drive, Columbus, OH 43205-2696, United States |
Abstract: | ![]() The p53-related p73 protein is an important mediator of apoptosis, development and tumorigenesis. Previously, we showed that over-expression of the p73β isoform induced apoptosis in proliferating neuronal cells; however, the study did not address the effect of p73 in post-mitotic neurons. To address this question, we used post-mitotic hNT neurons, which have been used as a model of human central nervous system neurons. We found that over-expression of p73β in hNT neurons resulted in apoptosis and an increase in the expression of p57Kip2 and Bax, but no increase in p53 expression. These results suggest that apoptosis of post-mitotic neurons induced by p73β may involve these mediators. Understanding the regulation of p73 expression will be important for understanding the development of the nervous system and may have implications for the treatment of neurological diseases. |