Catalog: | C-FC-2843A |
Product Type: | FCM Antibody |
Size: | 25 Tests/100 Tests |
Concentration: | 10 μl/Test, 0.1 mg/ml |
Reactivity: | Human |
Specificity: | Human BID |
Analysis mode: | FCM |
Host: | Mouse |
Clonality: | Monoclonal |
Isotype: | IgG1 |
Alternate names: | BH3 interacting domain death agonist |
Form: | Liquid |
Shipping: | This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. |
Storage: | This antibody can be stored at 2℃-8℃ for twelve months without detectable loss of activity. Protected from prolonged exposure to light. Do not freeze ! Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal. |
Purification method: | Protein A |
Conjugation: | FITC |
Immunogen: | Recombinant Human BID protein |
Buffer: | Aqueous solution containing 0.5% BSA and 0.09% sodium azide |
The BH3 interacting domain death agonist (BID) is a pro-apoptotic member of the Bcl-2 protein family, which contains only the BH3 domain, and is required for its interaction with the Bcl-2 family proteins and for its pro-death activity. BID is important to cell death mediated by these proteases and thus is the sentinel to protease-mediated death signals. Recent studies further indicate that Bid may be more than just a killer molecule, it could be also involved in the maintenance of genomic stability by engaging at mitosis checkpoint. BID is an integrating key regulator of the intrinsic death pathway that amplifies caspase-dependent and caspase-independent execution of neuronal apoptosis. Therefore pharmacological inhibition of BID provides a promising therapeutic strategy in neurological diseases where programmed cell death is prominent. BID is activated by Caspase 8 in response to Fas/TNF-R1 death receptor activation. Activated BID is translocated to mitochondria and induces cytochrome c release, which in turn activates downstream caspases. BID action has been proposed to involve the mitochondrial re-location of its truncated form, tBid, to facilitate the release of apoptogenic proteins like cytochrome c.
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