Product Pathways - Apoptosis
Bcl-w (31H4) Rabbit mAb #2724
|2724S||100 µl (10 western blots)||---||In Stock||---|
|2724||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Mouse, Rat||Endogenous||18||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting
Specificity / Sensitivity
Bcl-w (31H4) Rabbit mAb detects endogenous levels of total Bcl-w protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding alanine 39 of Bcl-w.
Western blot analysis of extracts from A673 and C2C12 cell lines, using Bcl-w (31H4) Rabbit mAb.
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 (1-3). 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 (4). 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 (5). 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.
The pro-survival protein Bcl-w was originally identified in a PCR-based strategy aimed at discovering novel Bcl-2 family members and was found to be expressed in cells of myeloid origin, as well as many other tissues (6,7). Most tissues from bcl-w knockout mice were unaffected, but male mice did show defects in seminiferous tubule organization and spermatogenogenesis (8,9).
- Cory, S. et al. (2003) Oncogene 22, 8590-607.
- Antonsson, B. and Martinou, J.C. (2000) Exp Cell Res 256, 50-7.
- Sharpe, J.C. et al. (2004) Biochim Biophys Acta 1644, 107-13.
- Korsmeyer, S.J. et al. (1993) Semin Cancer Biol 4, 327-32.
- Bouillet, P. and Strasser, A. (2002) J Cell Sci 115, 1567-74.
- Gibson, L. et al. (1996) Oncogene 13, 665-75.
- O'Reilly, L.A. et al. (2001) Cell Death Differ 8, 486-94.
- Print, C.G. et al. (1998) Proc Natl Acad Sci U S A 95, 12424-31.
- Ross, A.J. et al. (1998) Nat Genet 18, 251-6.
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For Research Use Only. Not For Use In Diagnostic Procedures.
Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.
This antibody is developed, validated, and produced by CST using in part technology under license (granting certain rights including those under U.S. Patents No. 5,675,063 and 7,429,487) from Epitomics, Inc.