| Product Includes | Product # | Quantity | Mol. Wt | Isotype/Source |
|---|---|---|---|---|
| Bad (D24A9) Rabbit mAb | 9239 | 20 µl | 23 kDa | Rabbit IgG |
| Phospho-Bad (Ser112) (40A9) Rabbit mAb | 5284 | 20 µl | 23 kDa | Rabbit IgG |
| Bax (D2E11) Rabbit mAb | 5023 | 20 µl | 20 kDa | Rabbit IgG |
| Bik Antibody | 4592 | 20 µl | 20 kDa | Rabbit |
| Bim (C34C5) Rabbit mAb | 2933 | 20 µl | 12, 15, 23 kDa | Rabbit IgG |
| BID Antibody | 2002 | 20 µl | 15, 22 kDa | Rabbit |
| Bak (D4E4) Rabbit mAb | 12105 | 20 µl | 25 kDa | Rabbit IgG |
| Puma (D30C10) Rabbit mAb | 12450 | 20 µl | 23 kDa | Rabbit IgG |
| Anti-rabbit IgG, HRP-linked Antibody | 7074 | 100 µl | Goat |
Please visit cellsignal.com for individual component applications, species cross-reactivity, dilutions, protocols, and additional product information.
Description
The Pro-Apoptosis Bcl-2 Family Antibody Sampler Kit provides an economical means to examine several members of the Bcl-2 family and their activation status. The kit contains enough primary and secondary antibodies to perform two Western blot experiments per primary antibody.
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.
Bad is a pro-apoptotic member of the Bcl-2 family that can displace Bax from binding to Bcl-2 and Bcl-xL, resulting in cell death (6,7). Survival factors such as IL-3 can inhibit the apoptotic activity of Bad by activating intracellular signaling pathways that result in the phosphorylation of Bad at Ser112 and Ser136 (7). Phosphorylation at these sites results in the binding of Bad to 14-3-3 proteins and the inhibition of Bad binding to Bcl-2 and Bcl-xL (7). Akt has been shown to promote cell survival via its ability to phosphorylate Bad at Ser136 (8,9). Ser112 has been shown to be the substrate in vivo and in vitro of p90RSK (10,11) and mitochondria-anchored PKA (12).
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- 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.
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- Yang, E. et al. (1995) Cell 80, 285-91.
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- Datta, S.R. et al. (1997) Cell 91, 231-41.
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- Tan, Y. et al. (1999) J Biol Chem 274, 34859-67.
- Harada, H. et al. (1999) Mol Cell 3, 413-22.
Background References
Trademarks and Patents
Limited Uses
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