Recombinant Mouse BID Protein (His & GST Tag)(Active) | PKSM040720

Recombinant Mouse BID Protein (His & GST Tag)(Active) | PKSM040720 | Gentaur US, UK & Europe Disrtribition

Synonyms: 2700049M22Rik;AI875481;AU022477

Active Protein: Active protein

Activity: 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.

Protein Construction: 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.

Fusion Tag: N-His-GST

Species: Mouse

Expressed Host: E.coli

Shipping: This product is provided as lyophilized powder which is shipped with ice packs.

Purity: > 95 % as determined by reducing SDS-PAGE.

Endotoxin: Please contact us for more information.

Stability and 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.

Molecular Mass: 50 kDa

Formulation: Lyophilized from sterile 50mM Tris, 150mM NaCl, pH 7.5

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.

Research Area: N/A