Bax is a protein of the bcl-2 gene family. It promotes apoptosis by competing with bcl-2 proper. The Bax gene contains a small promoter element that complements a binding domain on the multi-faceted p53 tumor suppressor. Wild-type p53 has been demonstrated to upregulate the transcription of a chimeric reporter plasmid, utilizing the consensus promoter sequence of Bax approx. 50-fold over mutant p53. Mutations in this consensus sequence eliminate transcription of the reporter gene. Thus, it is likely that p53 promotes Bax’s apoptotic faculties in vivo as a primary transcription factor. Bax exerts a pro-apoptotic rather than an anti-apoptotic effect on cells. Bax targets mitochondrial mem-branes, inducing mitochondrial damage and cell death in a caspase-independent manner. Bad plays a critical role in the Bax-mediated apoptosis pathway by dimerizing with BclxL, causing the displacement of Bax. The displacement of Bax allows apoptosis to proceed.
Clone
2D2
Isotype
IgG1k
Host species
Mouse
Species Reactivity
Human, monkey
Cellular Localization
cytoplasm
Positive Control
Hodgkin’s lymphoma
Applications
Flow Cyt., IF, IHC, WB
Intended Use
Research Use Only