|Application ||WB, IHC, IP|
|Calculated MW||21995 Da|
|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|
|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|
|Precautions||Bid Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||The major proteolytic product p15 BID allows the release of cytochrome c (By similarity). Isoform 1, isoform 2 and isoform 4 induce ICE-like proteases and apoptosis. Isoform 3 does not induce apoptosis. Counters the protective effect of Bcl-2.|
|Cellular Location||Cytoplasm. Mitochondrion membrane. Note=When uncleaved, it is predominantly cytoplasmic. BH3-interacting domain death agonist p13: Mitochondrion membrane. Note=Associated with the mitochondrial membrane. Isoform 3: Cytoplasm.|
|Tissue Location||Isoform 2 and isoform 3 are expressed in spleen, bone marrow, cerebral and cerebellar cortex. Isoform 2 is expressed in spleen, pancreas and placenta (at protein level) Isoform 3 is expressed in lung, pancreas and spleen (at protein level). Isoform 4 is expressed in lung and pancreas (at protein level).|
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Provided below are standard protocols that you may find useful for product applications.
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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