Bax (D2E11) Rabbit Antibody
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Bax (D2E11) Rabbit Antibody

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CAT. NO.: AMA-0359

Target Information
UniProt ID Q07812
Product Details
Size 20 µL/100 µL
Reactivity Human
Host Rabbit
Source/Isotype Rabbit IgG
Storage Store at -20°C. Do not aliquot the antibody.
Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu45 of human Bax protein.
Usage
Application WB, IP, IHC
Product Usage Information Dilution Western Blotting (1:1000); Immunoprecipitation (1:100); Immunohistochemistry (1:50-1:200)
MW (Target) 20 kDa
Background
The Bcl-2 family consists of a number of evolutionarily conserved proteins containing Bcl-2 homology domains (BH) that regulate apoptosis through control of mitochondrial membrane permeability and release of cytochrome c Four BH domains have been identified (BH1-4) that mediate protein interactions. The family can be separated into three groups based upon function and sequence homology: pro-survival members include Bcl-2, Bcl-xL, Mcl-1, A1 and Bcl-w; pro-apoptotic proteins include Bax, Bak and Bok; and "BH3 only" proteins Bad, Bik, Bid, Puma, Bim, Bmf, Noxa and Hrk. Interactions between death-promoting and death-suppressing Bcl-2 family members has led to a rheostat model in which the ratio of pro-apoptotic and anti-apoptotic proteins controls cell fate Thus, pro-survival members exert their behavior by binding to and antagonizing death-promoting members. In general, the "BH3-only members" can bind to and antagonize the pro-survival proteins leading to increased apoptosis While some redundancy of this system likely exists, tissue specificity, transcriptional and post-translational regulation of many of these family members can account for distinct physiological roles.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.

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