Bax Involvement in p53-Mediated Neuronal Cell Death

• DOI: 10.1523/jneurosci.18-04-01363.1998
• Publication Date: 2018-04-03T03:05:41Z
• Authors: Hong Xiang; Yoshito Kinoshita; C. Michael Knudson; Stanley J. Korsmeyer; Philip A. Schwart...; Richard S. Morrison
• Keywords: Viability assay; Bcl-2-associated X protein

The tumor suppressor gene p53 has been implicated in the loss of neuronal viability, but signaling events associated with p53-mediated cell death cortical and hippocampal neurons are not understood. Previous work shown that adenovirus-mediated delivery causes some features typical apoptosis. In present study we determined whether p53-initiated changes viability were dependent on members Bcl-2 family regulators. Primary cultures derived from animals containing Bax (+/+ +/-) or those deficient (-/-). Cell damage was assessed by direct counting measurements MTT activity. Neurons at least one copy damaged severely exposure to excitotoxins induction DNA damage. contrast, Bax-deficient (-/-) exhibited significant protection both types injury. protein expression elevated significantly glutamate exposure, camptothecin-induced wild-type neurons. glutamate-induced increase presence gene. However, increased expression, using transduction, sufficient itself elevate levels. These results demonstrate is required for response forms cytotoxic injury further support key role activation excitotoxic genotoxic