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mouse BAD Antibody (Center S112/S111/Y113)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | Q61337 |
| Other Accession | O35147, NP_031548.1 |
| Reactivity | Mouse |
| Predicted | Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 22080 Da |
| Antigen Region | 90-118 aa |
| Gene ID | 12015 |
|---|---|
| Other Names | Bcl2-associated agonist of cell death, BAD, Bcl-2-binding component 6, Bcl-xL/Bcl-2-associated death promoter, Bcl2 antagonist of cell death, Bad, Bbc6 |
| Target/Specificity | This mouse BAD antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 90-118 amino acids from the Central region of mouse BAD. |
| Dilution | WB~~1:1000 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | mouse BAD Antibody (Center S112/S111/Y113) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | Bad |
|---|---|
| Synonyms | Bbc6 |
| Function | Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. |
| Cellular Location | Mitochondrion outer membrane. Cytoplasm. Note=Colocalizes with HIF3A isoform 2 in the cytoplasm (PubMed:21546903). Upon phosphorylation, locates to the cytoplasm. |
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Provided below are standard protocols that you may find useful for product applications.
Background
BAD promotes cell death. It successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways.
References
Santidrian, A.F., et al. Blood 116(16):3023-3032(2010)
Frenzel, A., et al. Blood 115(5):995-1005(2010)
Quoyer, J., et al. J. Biol. Chem. 285(3):1989-2002(2010)
Polzien, L., et al. J. Biol. Chem. 284(41):28004-28020(2009)
Wu, X., et al. Diabetologia 52(10):2130-2141(2009)
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