| CatalogCode: | NSB436 |
| ProductName: | Bid Cleavage Site Antibody |
| Product Description: | Rabbit Polyclonal anti-Bid Cleavage Site |
| Clonality: | Polyclonal |
| Immunogen: | Synthetic peptide (Mouse)corresponding to N-terminus of cleavage site (59/60). |
| CrossReactivity: | Works in mouse. Does not cross-react with Human. Not yet tested in other species. |
| Packaging: | 0.1 ml Immunogen affinity purified Rabbit antisera. |
| Uses: | WB: Use at a concentration of 0.25 - 1.0 ug/ml. Predicted molecular weight: 15 kDa. Not tested in other applications. Optimal dilutions/concentrations should be determined by the end user. |
| Localization: | Cytoplasmic in its inactive form and translocates onto mitochondria once cleaved. |
| Control: | TNF alpha treated L929 cells. |
| Background: | BH3 interacting domain death agonist (BID) is a pro-apoptotic member of the Bcl 2 family. BID interacts with both Bcl 2 and Bax through its BH3 domain. It usually exists in an inactive form in the cytosolic fraction of living cells and becomes cleaved and activated by caspase 8 in response to TNF alpha or Fas ligand. Once BID is cleaved, the C-terminal 15 kDa fragment of BID (p15) translocates onto mitochondria and is sufficient to trigger cytochrome c release, resulting in cell apoptosis. BID serves as a direct molecular link between caspase 8 activation and mitochondrial death machinery. |
| Storage: | Aliquot and store at -20C or -80C. Avoid freeze-thaw cycles. |
| Purity: | Immunogen affinity purified |
| Isotype: | IgG |
| Host_Name: | Rabbit |
| Buffer: | Preservative: 0.1% Sodium Azide Constituents: 1% BSA, PBS. pH 7.2 |
| ListPrice: | 325 |
| AppSummary: | WB |
| SpeciesSummary: | Ha(-), Mu |
| ProteinTarget: | Bid Cleavage Site |
| PackageSize: | 0.1 ml |
| GeneralRef: | <b>General / background references:</b>Tan KO <i>et al.</i> A novel BH3-like domain in BID is required for intramolecular interaction and autoinhibition of pro-apoptotic activity. <i>J Biol Chem</i> <b>274</b>:23687-90 (1999). <PUBMED:10446124>Gross A <i>et al.</i> Caspase cleaved BID targets mitochondria and is required for cytochrome c release, while BCL-XL prevents this release but not tumor necrosis factor-R1/Fas death. <i>J Biol Chem</i> <b>274</b>:1156-63 (1999). <PUBMED:9873064>Luo X <i>et al.</i> Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors. <i>Cell</i> <b>94</b>:481-90 (1998). <PUBMED:9727491>Li H <i>et al.</i> Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis. <i>Cell</i> <b>94</b>:491-501 (1998). <PUBMED:9727492>Wang K <i>et al.</i> BID: a novel BH3 domain-only death agonist. <i>Genes Dev</i> <b>10</b>:2859-69 (1996). <PUBMED:8918887> Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis. <i>Nature</i> <b>400</b>:886-891 (0). Yin, X.M., et al. (1999) Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis. Nature. 400:886-891. |