|Datasheet||Specific References||Reviews||Related Products||Protocols|
|2700049M22Rik, AI875481, AU022477|
|A DNA sequence encoding the mature form of mouse BID (EDK99650.1) (Met 1-Asp 195) was fused with the N-terminal polyhistidine-tagged GST tag at the N-terminus.|
|In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.|
Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.
|> 95 % as determined by SDS-PAGE|
|1. Measured by its binding ability in a functional ELISA.|
2. Immobilized mouse BID at 10 μg/mL (100 μl/well) can bind biotinylated human BCL2L1, The EC50 of biotinylated human BCL2L1 is 7.01 ng/mL.
3. Immobilized mouse BID at 10 μg/mL (100 μl/well) can bind biotinylated mouse BCL2L1, The EC50 of biotinylated mouse BCL2L1 is 7.1 ng/mL.
|Please contact us for more information.|
|Samples are stable for up to twelve months from date of receipt at -70℃|
|The recombinant mouse BID/GST chimera consisting of 435 amino acids and has a calculated molecular mass of 50 kDa. It migrates as a 47 kDa band in SDS-PAGE under reducing conditions.|
|Lyophilized from sterile 50mM Tris, 150mM NaCl, pH 7.5|
1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
2. Please contact us for any concerns or special requirements.
|Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.|
|A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.|
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.