Bax [ID3]

GWB-D1347C

IgG1

Human

Bax

0. 1 mg/ml

0. 2% Gelatin 50mM Sodium phosphate with 0. 1% sodium azide

21 kDa. For IP: Use at a concentration of 0. 5 - 1. 5 µ g/ml. Not suitable for use in IHC-Fr or IHC-P. Not tested in other applications. Optimal dilutions/concentrations should be determined by the researcher. Target protein

Cell Membrane Myeloma: Sp2/0 Bcl2 family is a key regulator of apoptosis that functions to either inhibit or promote cell death. Over-expression of members such as Bcl2 and BclxL inhibit the apoptotic process. The Bcl2 family members are also characterized by dimerizing to further modulate apoptosis. Bag1 for example has been found to form a heterodimer with Bcl2 resulting in the enhancement of the anti-apoptotic effect of Bcl2. Bax and Bak have been shown to play a critical role in cytochrome c release from mitochondria and thus initiate apoptosis. Bax exerts a pro-apoptotic rather than an anti-apoptotic effect on cells. Bax targets mitochondrial membranes 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 displacment of Bax. The displacement of Bax allows apoptosis to proceed. BclxS a shorter version of BclxL (lacking amino acids 126-188) apparently utilizes a different pathway than Bax to induce cell death. Some research suggests that BclxS uses a novel mechanism for regulating caspase or it may use an alternate cell death effector pathway.

Monomer. Homodimer and heterodimer with BCL2 E1B 19K protein BCL2L1 isoform Bcl-X(L) MCL1 and BCL2A1/A1. Interacts with SH3GLB1 and HN.

Isoform Beta: Cytoplasm.

Isoform Delta: Cytoplasm (Potential).

Intact BH3 motif is required by BIK BID BAK BAD and BAX for their pro-apoptotic activity and for their interaction with anti-apoptotic members of the Bcl-2 family (By similarity).

Belongs to the Bcl-2 family.