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Physiological functions of hBAX

Bax is a pro-apoptotic Bcl-2 protein. It promotes apoptosis by competing with Bcl-2 proper.

Upon initiation of apoptotic signaling, Bax undergoes a conformation shift, and inserts into organelle membranes, primarily the outer mitochondrial membrane.Bax is believed to interact with, and induce the opening of the mitochondrial voltage-dependent anion channel, VDAC. Alternatively, growing evidence suggest that activated Bax and/or Bak form an oligomeric pore, MAC in the outer membrane. This results in the release of cytochrome c and other pro-apoptotic factors from the mitochondria, often referred to as mitochondrial outer membrane permeabilization (MOMP), leading to activation of caspases.

Potential applications of hBAX

In our system we would like to induce apoptosis by increasing the amount of proapoptotic proteins such as BAX by producing an expression vector containing TRE-minimal CMV promoter, BAX or PUMA and polyA tail. The proapoptotic proteins are able to express only in a controlled form using the advanced Tet-On expression system. The overexpression of these proteins can lead to Mitochondrial Outer Membrane Permeabilisation (MOMP) which is a point of no return in the mitochondrial pathway of Programmed Cell Death (PCD). The goal is to “switch off” the cells, which were genetically modified by us, after they “finished their work” in the recent local environment combining the components of the tetracycline-inducible system in self-contained retroviral and plasmid vectors.

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