Wild type p53 is a transcriptional activator which plays a crucial role in the control of radiation induced apoptosis. Recent evidence suggests that p53 modulates apoptosis by upregulating the expression of Bax, a bcl-2 gene family member which functions to facilitate cell death. Importantly, Bax was only induced following radiation in cells which express wt p53. In the pediatric malignancy neuroblastoma (NB) p53 mutations are rare and most NB cell lines express wt p53. In previous studies we have determined that some NB cell lines fail to upregulate p53 following gamma radiation and are resistant to radiation induced apoptosis. Single gene transfection studies have demonstrated that induction of p53 beyond threshold levels following radiation can initiate apoptosis in NB cells. The aim of the present study was to study the kinetics of Bax induction following radiation in parental and p53 transfected NB cell lines. Western blot analysis of parental Shep-1 cells radiated at 25 Gy revealed Bax was induced and maximally expressed at 24 hours. This increase in Bax expression was seen in the absence of p53 induction. These same experiments were conducted in cell lines transfected with a temperature sensitive p53 expression construct. For these experiments cells were radiated at 25 Gy and p53 was pulse induced by placing cells at the permissive temperature(32.5°C). High level p53 expression was confirmed by quantitative immunoprecipitation. In contrast to parental cells, Shep-1 cells transfected with the temperature sensitive p53 expression construct failed to demonstrate any p53 dependent increase in Bax levels following radiation and high level p53 expression. These results suggest induction of Bax is not critical for radiation induced apoptosis in NB and that the pathway of p53-mediated apoptosis does not require Bax expression in this system.