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. (Shipping Cost: €200.00)

BAX [2D2]

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.

BAX [2D2]