BID Protein, Human, Recombinant is expressed in E. coli expression system. The predicted molecular weight is 22 kDa and the accession number is P55957-1.

Human

E. coli

FP497,BH3 interacting domain death agonist

A DNA sequence encoding the human BID isoform 1 (P55957-1) (Met 1-Asp 195) was expressed and purified, with additional two amino acids (Gly & Pro) at the N-terminus. Predicted N terminal: Met

> 90 % as determined by SDS-PAGE

A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.

It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.

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.