Expression data from BAX/BAK double knockout mouse embryonic fibroblast at baseline and following exposure to genotoxic stress.

The BCL-2 family proteins are central regulators of apoptosis. However, cells doubly deficient for BAX and BAK or overexpressing BCL-2 still succumb to oxidative stress upon DNA damage or loss of matrix attachment. Our studies indicate a central role for the transcription factor deltaNp63alpha (referred to as p63 from this point forward) in this form of non-apoptotic cell death. We used microarrays to investigate gene expression in apoptosis-incompetent cells expressing a control vector or p63, at baseline and following exposure to genotoxic stress, to further elucidate molecular mechanisms regulating this type of non-apoptotic death and the role of p63 in this context. SV40 transformed BAX/BAK double knockout (DKO) mouse embryonic fibroblasts were transduced with retrovirus expressing GFP or p63, then were mock-treated or treated with etoposide (10 micrograms/ul) for 6 hours prior to harvesting of mRNA for analysis with Affymetrix GeneChip Mouse Gene 1.0 ST. Four samples are included: DKO GFP mock treated, DKO GFP etoposide treated, DKO p63 mock treated, and DKO GFP etoposide treated