Bax is a key component for cellular induced apoptosis through mitochondrial stress. Upon apoptotic stimulation, Bax forms oligomers and translocates from the cytosol to the mitochondrial membrane. Through interactions with pore proteins on the mitochondrial membrane, Bax increases the membrane's permeability, which leads to the release of cytochrome c from mitochondria, activation of caspase-9 and initiation of the caspase activation pathway for apoptosis.

Apoptosis regulator BAX (Bcl-2-like protein 4) (Bcl2-L-4) BAX BCL2L4

Human Mouse Rat Hamster

WB,IHC,IP,FCM

WB 1:1000~1:2000 IHC 1:50~1:200 IP 1:50 FC 1:50

21kDa

BAX BCL2L4

q07812

https://www.uniprot.org/uniprotkb/q07812

A synthesized peptide derived from human Bax

Rabbit

Monoclonal

Rabbit IgG

Bax Antibody detects endogenous levels of total Bax

Apoptosis

Affinity-chromatography

PBS, pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol

Store at +4°C short term. Store at -20°C long term. Avoid freeze / thaw cycle.