BH3 Interacting Domain Death Agonist (BID) (AA 50-62) antibody
|Synonyms||FP497, MGC15319, MGC42355, AI875481, AU022477, 2700049M22Rik, BID, MGC140420, bid, si:ch211-238n5.6, xbid, fp497, DKFZp469E066|
Alternatives Western Blotting (WB), Immunofluorescence (IF)
|5 references available|
|Quantity||50 µg (250 µg/ml)|
|Price||Product not available in this region.|
|Description||Members of the Bcl-2 protein family function to inhibit (Bcl-2, Bcl-XL, Mcl-1, A1) or promote (Bax, Bak, Bcl-Ls, Bad) apoptosis. Bid is a Bcl-2 family death agonist that heterodimerizes with either agonists (Bax) or antagonists (Bcl-2). Bid contains a centrally located BH3 domain that allows interaction with the BH1 domain of Bax and Bcl-2. However, Bid does not contain other domains commonly found in Bcl-2 family members, such as BH1, BH2, or BH4. In addition, Bid does not contain a C-terminal hydrophobic region that is characteristic of membrane-bound Bcl-2 family members. Singlet oxygen-induced apoptosis in human leukemia cells and Fas-induced apoptosis involve caspase-8 cleavage of Bid, which produces a 15 kDa C-terminal fragment and a 6.5 kDa N-terminal fragment. The C-terminal fragment translocates to the mitochondria and promotes the release of cytochrome C through a mechanism that might involve destabilization of the mitochondrial membrane. Thus, the proapoptotic role of Bid may involve mitochondrial membrane destabilization, as well as multiple protein-protein interactions.|
1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2. Please refer to us for technical protocols.
3. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
4. Source of all serum proteins is from USDA inspected abattoirs located in the United States.
|Molecular Weight||23 kDa|
Related Products: ABIN968537, ABIN967389
|Purification||Purified from tissue culture supernatant or ascites by affinity chromatography.|
|Buffer||Aqueous buffered solution containing BSA, glycerol.|
|Preservative||0.09% Sodium azide.|
|Storage||Store undiluted at -20°C.|
|Research Area||Cancer, Apoptosis/Necrosis|
|Restrictions||For Research Use only|
Wang, Yin, Chao et al.: "BID: a novel BH3 domain-only death agonist." in: Genes & development, Vol. 10, Issue 22, pp. 2859-69, 1996 (PubMed).
Kudla, Montessuit, Eskes et al.: "The destabilization of lipid membranes induced by the C-terminal fragment of caspase 8-cleaved bid is inhibited by the N-terminal fragment." in: The Journal of biological chemistry, Vol. 275, Issue 30, pp. 22713-8, 2000 (PubMed).
Zhuang, Demirs, Kochevar: "p38 mitogen-activated protein kinase mediates bid cleavage, mitochondrial dysfunction, and caspase-3 activation during apoptosis induced by singlet oxygen but not by hydrogen peroxide." in: The Journal of biological chemistry, Vol. 275, Issue 34, pp. 25939-48, 2000 (PubMed).
Devarajan, De Leon, Talasazan et al.: "The von Hippel-Lindau gene product inhibits renal cell apoptosis via Bcl-2-dependent pathways." in: The Journal of biological chemistry, Vol. 276, Issue 44, pp. 40599-605, 2001 (PubMed).
Gómez-Angelats, Cidlowski: "Protein kinase C regulates FADD recruitment and death-inducing signaling complex formation in Fas/CD95-induced apoptosis." in: The Journal of biological chemistry, Vol. 276, Issue 48, pp. 44944-52, 2001 (PubMed).