Recombinant Human BID Protein (PKSH031587)
For research use only.
| Synonyms | BH3-Interacting Domain Death Agonist, BID, p22 BID |
| Species | Human |
| Expression Host | E.coli |
| Sequence | Met 1-Asp 195 |
| Accession | P55957-1 |
| Calculated Molecular Weight | 22 kDa |
| Observed Molecular Weight | 22 kDa |
| Tag | None |
| Bio-activity | 1. Immobilized human BID at 10 μg/mL (100 μl/well) can bind biotinylated human BCL2L1, The EC50 of biotinylated human BCL2L1 is 7.1 ng/mL. 2. Immobilized human BID at 10 μg/mL (100 μl/well) can bind biotinylated mouse BCL2L1, The EC50 of biotinylated mouse BCL2L1 is 5. 6 ng/mL. |
| Purity | > 90 % as determined by reducing SDS-PAGE. |
| Endotoxin | Please contact us for more information. |
| Storage | Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months. |
| Shipping | This product is provided as lyophilized powder which is shipped with ice packs. |
| Formulation |
Lyophilized from sterile 40mM Tris, 150mM NaCl, pH 8.0 Normally 5% - 8% trehalose, mannitol and 0.01% Tween 80 are added as protectants before lyophilization. Please refer to the specific buffer information in the printed manual. |
| Reconstitution | Please refer to the printed manual for detailed information. |
| Background | 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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