| Product Includes | Product # | Quantity | Mol. Wt | Isotype/Source |
|---|---|---|---|---|
| Phospho-Bcl-2 (Ser70) (5H2) Rabbit mAb | 2827 | 20 µl | 28 kDa | Rabbit IgG |
| Phospho-Bcl-2 (Thr56) Antibody | 2875 | 20 µl | 28 kDa | Rabbit |
| Bcl-2 (D55G8) Rabbit mAb | 4223 | 20 µl | 26 kDa | Rabbit IgG |
| Bcl-xL (54H6) Rabbit mAb | 2764 | 20 µl | 30 kDa | Rabbit IgG |
| Mcl-1 (D35A5) Rabbit mAb | 5453 | 20 µl | 40 (human), 35 (mouse) kDa | Rabbit IgG |
| Anti-rabbit IgG, HRP-linked Antibody | 7074 | 100 µl | Goat |
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Description
The Pro-Survival Bcl-2 Family Antibody Sampler Kit provides an economical means to examine several members of the Bcl-2 family. The kit contains enough primary and secondary antibodies to perform two western blot experiments.
Storage
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 (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.
Several phosphorylation sites have been identified within Bcl-2 including Thr56, Ser70, Thr74 and Ser87 (6). These phosphorylation sites may be targets of the ASK1/MKK7/JNK1 pathway, and phosphorylation of Bcl-2 may be a marker for mitotic events (7,8). Mutation of Bcl-2 at Thr56 or Ser87 inhibits its anti-apoptotic activity during glucocorticoid-induced apoptosis of T lymphocytes (9). Interleukin 3 and JNK-induced Bcl-2 phosphorylation at Ser70 may be required for its enhanced antiapoptotic functions (10).
- 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.
- Maundrell, K. et al. (1997) J Biol Chem 272, 25238-42.
- Yamamoto, K. et al. (1999) Mol Cell Biol 19, 8469-78.
- Ling, Y.H. et al. (1998) J Biol Chem 273, 18984-91.
- Huang, S.T. and Cidlowski, J.A. (2002) FASEB J 16, 825-32.
- Deng, X. et al. (2001) J Biol Chem 276, 23681-8.
Background References
Trademarks and Patents
Limited Uses
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