Product Pathways - Apoptosis
Bcl-w (31H4) Rabbit mAb #2724
|W||H M R||Endogenous||18||Rabbit IgG|
Reactivity Key: H=Human M=Mouse R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
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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Rabbit Monoclonals Produced Using Epitomics® Technology, U.S. Patent No. 5,675,063.
For Research Use Only. Not For Use In Diagnostic Procedures.