Bid Antibody
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, IHC, IP |
---|---|
Primary Accession | P70444 |
Reactivity | Mouse |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 21952 Da |
Gene ID | 12122 |
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Application & Usage | Western blot analysis (0.5-4 µg/ml), immunoprecipitation (5-10 µg/ml), and Immunohistochemistry (20-40 µg/ml). However, the optimal conditions should be determined individually. The antibody detects 22 kDa human Bid |
Other Names | FP497 , MGC42355, MGC15319 |
Target/Specificity | Bid |
Antibody Form | Liquid |
Appearance | Colorless liquid |
Formulation | 100 µg (0.5 mg/ml) affinity purified rabbit anti-Bid 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 | Bid Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | Bid |
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Function | Induces caspases and apoptosis. Counters the protective effect of BCL2. |
Cellular Location | Cytoplasm. Mitochondrion membrane. Mitochondrion outer membrane {ECO:0000250|UniProtKB:P55957}. Note=When uncleaved, it is predominantly cytoplasmic. [BH3-interacting domain death agonist p13]: Mitochondrion membrane. Note=Associated with the mitochondrial membrane. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Bid, a BH3 domain-containing proapoptotic Bcl-2 family member, is localized in the cytosolic fraction of cells as an inactive precursor. Its active form is generated upon proteolytic cleavage by caspase-8 in the Fas signaling pathway. Cleaved Bid translocates to mitochondria and releases its potent proapoptotic activity, which in turn induces cytochrome c release and mitochondrial damage. The cytochrome c releasing activity of Bid was antagonized by Bcl-2. Mutation in the SH3 domain can diminish the cytochrome c releasing activity. In the animal model studies, Bid-deficient mice are found resistant to the lethal effects of death factor signals relayed thro µgh Fas.
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