Bcl-xL Antibody
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, IP |
---|---|
Primary Accession | Q92934 |
Reactivity | Human, Mouse, Rat |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 18392 Da |
Gene ID | 572 |
---|---|
Application & Usage | Western blotting (0.5-4 µg/ml) and immunoprecipitation (20 µ/ml). However, the optimal conditions should be determined individually. The antibody detects the 30 kDa Bcl-xL protein. It does not react with other Bcl-2 family members. |
Other Names | Bcl-xL, Bcl-xS, BCL2L1, BCL2-like 1 protein |
Target/Specificity | Bcl-xl |
Antibody Form | Liquid |
Appearance | Colorless liquid |
Formulation | 100 µg (0.5 mg/ml) affinity purified, rabbit anti-Bcl-xL polyclonal antibody in phosphate buffered saline (PBS), pH 7.2, containing 30% glycerol, 0.5% BSA, 0.01% thimerosal. |
Handling | The antibody solution should be gently mixed before use. |
Reconstitution & Storage | -20 °C |
Background Descriptions | |
Precautions | Bcl-xL Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | BAD |
---|---|
Synonyms | BBC6, BCL2L8 |
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 (By similarity). Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. |
Cellular Location | Mitochondrion outer membrane. Cytoplasm {ECO:0000250|UniProtKB:Q61337}. Note=Colocalizes with HIF3A in the cytoplasm (By similarity). Upon phosphorylation, locates to the cytoplasm. {ECO:0000250|UniProtKB:Q61337} |
Tissue Location | Expressed in a wide variety of tissues. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Bcl-xL is a 30 kDa anti-apoptotic protein belonging to the Bcl-2 family. Bcl-xL prevents apoptosis thro µgh two different mechanisms: by heterodimerization with an apoptotic protein to inhibit its apoptotic effect, and by its direct pore-forming effect on the outer-membrane of mitochondria to help maintain a normal membrane state under stress conditions. Bcl-xL can be cleaved by caspases upon apoptotic activation, which converts Bcl-xL from an antiapoptotic protein to a proapoptotic cleavage product. The cleavage product of Bcl-xL forms cytochrome c-releasing pores in the mitochondrial membrane to facilitate the apoptosis signaling pathway.
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