Phospho-mouse BAD(S96) Antibody
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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Application ![]()
| DB, E |
---|---|
Primary Accession | Q61337 |
Other Accession | NP_031548.1 |
Reactivity | Mouse |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 22080 Da |
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 phosphopeptide corresponding to amino acid residues surrounding S96 of mouse BAD. |
Dilution | DB~~1:500 E~~Use at an assay dependent concentration. |
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 | Phospho-mouse BAD(S96) Antibody 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. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
BAD 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.
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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