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J Neurol Sci. 2006 Jan 15;240(1-2):1-6. Epub 2005 Oct 5.

Over-expression of p73beta results in apoptotic death of post-mitotic hNT neurons.

Author information

1
Center for Childhood Cancer, Children's Research Institute, Division of Neurology, Children's Hospital, The Ohio State University, College of Medicine and Public Health, 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 p73beta 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 p73beta 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 p73beta 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.

PMID:
16212980
DOI:
10.1016/j.jns.2005.08.012
[Indexed for MEDLINE]

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