Recombinant Human BID Protein (Active) | PKSH031587

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SKU:
575-PKSH031587
€998.00
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Description

Recombinant Human BID Protein (Active) | PKSH031587 | Gentaur US, UK & Europe Disrtribition

Synonyms: BH3-Interacting Domain Death Agonist; p22 BID; BID

Active Protein: Active protein

Activity: 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.

Protein Construction: 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.

Fusion Tag: N/A

Species: Human

Expressed Host: E.coli

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

Purity: > 90 % 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: N/A

Formulation: Lyophilized from sterile 40mM Tris, 150mM NaCl, pH 8.0

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

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