Key features and details
- Rabbit polyclonal to Bid Cleavage Site
- Suitable for: WB
- Reacts with: Mouse, Human
- Isotype: IgG
Product nameAnti-Bid Cleavage Site antibody
See all Bid Cleavage Site primary antibodies
DescriptionRabbit polyclonal to Bid Cleavage Site
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Mouse, Human
Synthetic peptide (Mouse)corresponding to N-terminus of cleavage site (59/60).
- TNF alpha treated L929 cells.
BH3 interacting domain death agonist (BID) is a pro-apoptotic member of the Bcl 2 family. BID interacts with both Bcl 2 and Bax through its BH3 domain. It usually exists in an inactive form in the cytosolic fraction of living cells and becomes cleaved and activated by caspase 8 in response to TNF alpha or Fas ligand. Once BID is cleaved, the C-terminal 15 kDa fragment of BID (p15) translocates onto mitochondria and is sufficient to trigger cytochrome c release, resulting in cell apoptosis. BID serves as a direct molecular link between caspase 8 activation and mitochondrial death machinery.
Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Storage bufferpH: 7.30
Preservative: 0.05% Sodium azide
Constituents: PBS, 1% BSA, 50% Glycerol
Concentration information loading...
PurityImmunogen affinity purified
Purification notesPurified from rabbit serum by epitope-specific affinity chromatography.
Primary antibody notesBH3 interacting domain death agonist (BID) is a pro-apoptotic member of the Bcl 2 family. BID interacts with both Bcl 2 and Bax through its BH3 domain. It usually exists in an inactive form in the cytosolic fraction of living cells and becomes cleaved and activated by caspase 8 in response to TNF alpha or Fas ligand. Once BID is cleaved, the C-terminal 15 kDa fragment of BID (p15) translocates onto mitochondria and is sufficient to trigger cytochrome c release, resulting in cell apoptosis. BID serves as a direct molecular link between caspase 8 activation and mitochondrial death machinery.
Our Abpromise guarantee covers the use of ab10640 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 0.5 - 1 µg/ml. Predicted molecular weight: 15 kDa.|
RelevanceBid, 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.
- Apoptic death agonist antibody
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Mouse L929 cells were treated with 5
µg/mL actinomycin plus 2.5 ng/mL, 5 ng/mL and 10 ng/mL mouse TNF alpha for 5 hours (Lane 3, 4 and 5). Untreated L929 cells (Lane 1) and cells treated with actinomycin alone (Lane 2) were used as controls. Proteins were resolved from the cells by SDS-PAGE. The proteins were transferred to PVDF membranes. The membranes were incubated with the anti-mouse full length BID antibody (left panel) and ab10640 (right panel) at 1 µg/mL. The signal was detected using a goat F(ab’)2 anti-rabbit IgG alkaline phosphatase antibody at a 1/5000 dilution and the membrane was incubated with CDP-substrate followed by chemiluminescence. The data show that ab10640 only recognizes the cleaved mouse BID and not full length (Right panel). The full length BID was revealed using an anti-mouse full length BID antibody (Left panel). Mouse L929 cells were treated with 5 µg/mL actinomycin plus 2.5 ng/mL, 5 ng/mL and 10
ab10640 has been referenced in 11 publications.
- Yen JH et al. Activation of dynamin-related protein 1 - dependent mitochondria fragmentation and suppression of osteosarcoma by cryptotanshinone. J Exp Clin Cancer Res 38:42 (2019). PubMed: 30691497
- Liao Y et al. Endoplasmic Reticulum Stress Induces Macrophages to Produce IL-1ß During Mycobacterium bovis Infection via a Positive Feedback Loop Between Mitochondrial Damage and Inflammasome Activation. Front Immunol 10:268 (2019). PubMed: 30846986
- Chung TW et al. Antitumor effect of kurarinone and underlying mechanism in small cell lung carcinoma cells. Onco Targets Ther 12:6119-6131 (2019). PubMed: 31496721
- Li Q et al. Chemically modified liposomes carrying TRAIL target activated hepatic stellate cells and ameliorate hepatic fibrosis in vitro and in vivo. J Cell Mol Med N/A:N/A (2018). PubMed: 30592139
- Zeng X et al. Acylated and unacylated ghrelin inhibit apoptosis in myoblasts cocultured with colon carcinoma cells. Oncol Rep 39:1387-1395 (2018). PubMed: 29328480