Background:

BID, a BH3 domain containing proapoptotic Bcl2 family member, is localized in the cytosolic fraction of cells as an inactive precursor. Its active form is generated upon proteolytic cleavage by caspase 8 in the Fas signaling pathway. Cleaved Bid translocates to mitochondria and releases its potent proapoptotic activity, which in turn induces cytochrome c release and mitochondrial damage. The cytochrome c releasing activity of Bid was antagonized by Bcl2. Mutation in the SH3 domain can diminish the cytochrome c releasing activity. In animal model studies, Bid deficient mice are found resistant to the lethal effects of death factor signals relayed through Fas.

Specificity:

BID mAb detects endogenous levels of BID protein.

Alternative names:

BH3-interacting domain death agonist; p22 BID; BID; BH3-interacting domain death agonist p15; p15 BID; BH3-interacting domain death agonist p13; p13 BID;,BH3-interacting domain death agonist p11; p11 BID; BID

Species reactivity:

Human

Host:

Mouse

Ig type:

1mg/ml in PBS with 0.02% sodium azide, 50% glycerol, pH7.2

Immunogen:

Recombinant full length Human BID.

Purification & Purity:

The antibody was affinity-purified from mouse ascites by affinity-chromatography using epitope-specific immunogen and the purity is > 95% (by SDS-PAGE).

Molecular weight:

Predicted band size:22KDa Observed band size:22KDa

Applications:

WB ICC

Usage:

WB: 1:300~1000 ICC: 1:100

Storage:

Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze-thaw cycles.

Precautions:

For research use only, not for use in diagnostic procedure.

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