Accelerates programmed cell death by binding to, and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis.1) Francesca Andriani. J Natl Cancer Inst, Sep 2001; 93: 1314 - 1324.
Immunogen
Bax (phospho Thr167) antibody was raised against a peptide sequence around phosphorylation site of threonine167 (P-G-T (p)-P-T) derived from Human Bax.