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BID Antibody (PE), Mouse MAb

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Human BID Antibody Product Information
Immunogen:Recombinant Human BID protein (Catalog#10468-HNCE)
Clone ID:10
Ig Type:Mouse IgG1
Concentration:5 μl/Test, 0.1 mg/ml
Formulation:Aqueous solution containing 0.5% BSA and 0.09% sodium azide
Preparation:This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human BID (rh BID; Catalog#10468-HNCE; P55957-1; Met 1-Asp 195) and conjugated with PE under optimum conditions, the unreacted PE was removed.
Human BID Antibody Usage Guide
Specificity:Human BID
No cross-reactivity in ELISA with
E.coli cell lysate
Storage:This antibody is stable for 12 months from date of receipt when stored at 2℃-8℃. Protected from prolonged exposure to light. Do not freeze !
Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.
Human BID Antibody FC Application Image
[Click to enlarge image]
Human BID expression in Jurkat cells. The cells were treated according to manufacturer’s manual (BD Pharmingen™ Cat. No. 554714), and then stained with PE Mouse anti-BID. The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.
BID Antibody (PE), Mouse MAb, Flow cytometric
Other BID Antibody Products
p22 BID 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.

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