PBS with 0.1% sodium azide and 0.2% gelatin
Store as concentrated solution. Centrifuge briefly prior to opening vial. Store at 4ºC. DO NOT FREEZE.
0.2 mg/ml (Please refer to the vial label for the specific concentration.)
Synthetic peptide (Human) (N terminal).
For laboratory use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Bcl2, Apoptosis Regulator,Bcl-2,Ppp1R50,Bcl2
Endoplasmic reticulum, outer mitochondrial membrane and nuclear membrane.
Bcl-2 family is a key regulator of apoptosis that function to either inhibit or promote cell death. Over expression of members such as Bcl-2 and Bcl-xL inhibit the apoptotic process (1,2). The Bcl-2 family members are also characterized by dimerizing to further modulate apoptosis. Bag-1, for example, has been found to form a heterodimer with Bcl-2 resulting in the enhancement of the anti-apoptotic effect of Bcl-2 (3,4). Bax and Bak have been shown to play a critical role in cytochrome c release from mitochondria and thus initiate apoptosis (6). Bad plays a critical role in the Bax-mediated apoptosis pathway by dimerizing with Bcl-xL, causing the displacement of Bax. The displacement of Bax allows apoptosis to proceed (7). Bcl-xS, a shorter version of Bcl-xL (lacking amino acids 126-188), apparently utilizes a different pathway than Bax to induce cell death. Some research suggests that Bcl-xS uses a novel mechanism for regulating caspase or it may use an alternate cell death effector pathway (8,9).