Detection of Human BID by Western Blot. Western blot shows Jurkat human acute T cell leukemia cell line treated with apoptosis inducer anti-Fas for the indicated times. PVDF membrane was probed with 1 µg/mL Goat Anti-Human/Mouse BID Antigen Affinity-purified Polyclonal Antibody (Catalog # AF860) followed by HRP-conjugated Anti-Goat IgG Secondary Antibody (Catalog # HAF109). A specific band was detected for BID at approximately 20 kDa (as indicated). For additional reference short (5 seconds, left panel) and long (60 seconds, right panel) exposures are shown. This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 2.
Detection of Human BID by Simple WesternTM. Simple Western lane view shows lysates of Jurkat human acute T cell leukemia cell line, loaded at 0.2 mg/mL. A specific band was detected for BID at approximately 29 kDa (as indicated) using 10 µg/mL of Goat Anti-Human/Mouse BID Antigen Affinity-purified Polyclonal Antibody (Catalog # AF860) followed by 1:50 dilution of HRP-conjugated Anti-Goat IgG Secondary Antibody (Catalog # HAF109). This experiment was conducted under reducing conditions and using the 12-230 kDa separation system.
Preparation and Storage
Reconstitute at 0.2 mg/mL in sterile PBS.
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
6 months, -20 to -70 °C under sterile conditions after reconstitution.
BID is a 195 amino acid member of the Bcl-2 family of proteins that regulates outer mitochondrial membrane permeability (1). BID is a pro-apoptotic member that causes cytochrome c to be released from the mitochondria intermembrane space into the cytosol. In healthy cells BID is cytosolic. In response to Fas ligand or TNF, BID is cleaved by caspase-8 and it then relocates to the mitochondria outer membrane (2, 3). Cleavage of BID by caspase-8 generates a new N-terminal that contains a terminal glycine. It appears that the glycine is myristoylated and myristoylation serves to target BID to the mitochondria (4). BID may then interact with another pro-apoptotic Bcl-2 family member Bak (5). Interaction of BID with Bak causes altered mitochondrial membrane permeability. A 9‑13 amino acid stretch called the BH3 region (Bcl-2 homology region) appears to mediate the BID interaction with other Bcl-2 family members. BID is neutralized by binding to the anti-apoptotic member Bcl-xL.
Gross, A. et al. (1999) Genes and Develop. 13:1899.
Luo, X., et al. (1998) Cell 94:481.
Li, H. et al. (1998) Cell 94:491.
Zha, J. et al. (2000) Science 290:1761.
Wei, M.C. et al. (2000) Genes Dev. 14:2060.
BH3 Interacting Domain Death Agonist
Entrez Gene IDs:
637 (Human); 12122 (Mouse)
apoptic death agonist; BH3 interacting domain death agonist; BH3-interacting domain death agonist; BID isoform ES(1b); BID isoform L(2); BID isoform Si6; desmocollin type 4; FP497; Human BID coding sequence; MGC15319; MGC42355; p22 BID
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The data collected includes not only links to publications in PubMed,
but also provides information about sample types, species, and experimental conditions.
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