- CITATIONS: 2
|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Other Names||BAX, BCL2L4, Apoptosis regulator BAX, Bcl-2-like protein 4|
|Target/Specificity||A synthetic peptide corresponding to residues in the vicinity of the dimerization domain of human Bax was used as immunogen. The antibody should recognize cytoplasmic isoform beta, delta, and membrane isoform alpha of Bax. The antibody does not cross-react with other Bcl-2 family members. Predicted to cross-react with bovine based on sequence homology.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Bax Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
Provided below are standard protocols that you may find useful for product applications.
Bax is a pro-apoptotic member of the Bcl-2 family of proteins. During mitochondria-regulated programmed cell death, Bax promotes apoptosis by binding Bcl-2 and inhibiting its anti-apoptotic function (1). Upon apoptotic stimulation, Bax translocates from the cytosol to the mitochondrial membrane (2). Through interactions with mitochondrial membrane proteins, Bax increases the membrane's permeability, leading to the release of cytochrome c from mitochondria and initiation of the apoptotic caspase cascade (2,3).
1. Oltvai, Z.N., et al. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death. Cell 74: 609
2. Jurgensmeier, J.M., et al. Bax directly induces release of cytochrome c from isolated mitochondria. Proc. Natl. Acad. Sci. USA 95: 4997
3. Narita, M., et al. Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria. Proc. Natl. Acad. Sci. USA 95: 14681
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