Fas (TNFRSF6)-Associated Via Death Domain (FADD) antibody

Details for Product No. ABIN967524
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Antigen
Synonyms MORT1, Mort1/FADD, Mort1, TNFRSF6
Reactivity
Human
(123), (57), (33), (12), (3), (2), (1)
Host
Mouse
(125), (41), (2)
Clonality (Clone)
Monoclonal ()
Conjugate
Un-conjugated
(4), (4), (4), (4), (4), (4), (4), (4), (4), (4), (4), (4)
Application
Western Blotting (WB), Immunoprecipitation (IP)
(116), (76), (40), (36), (24), (17), (8), (6), (2), (2), (2), (1), (1)
Pubmed 2 references available
Catalog no. ABIN967524
Quantity 0.1 mg
Price
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Immunogen Human FADD GST
Clone A66-2
Isotype IgG1
Characteristics 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.
Purification Purified from tissue culture supernatant or ascites by affinity chromatography.
Purity Purified
Alternative Name FADD
Background FADD is a molecule involved in the Fas-mediated cell death pathway. Apoptosis is induced when Fas ligand or agonistic Fas antibodies bind to the Fas receptor, and trigger the activation of a cell death signaling pathway. Induction of Fas-mediated apoptosis requires a conserved cytoplasmic motif, referred to as the death domain, that is present in the C-terminal end of Fas. FADD also contains a death domain, and Fas and FADD bind to each other through their respective death domains. Death domains are thought to act as adaptor proteins by linking Fas and other members of the tumor necrosis factor receptor (TNFR) superfamily to downstream signaling pathways. Overexpression of FADD in vitro leads to cell death suggesting that FADD, like FAS, is an apoptosis-inducing protein. The N-terminal, but not the C-terminal death domain, is required for apoptosis induced by FADD overexpression. It is thought that the amino-terminal region of FADD functions by binding to caspase-3 and thereby linking signals from the cell surface to an apoptopic protease cascade. FADD has a calculated molecular weight of 24 kDa and migrates at a molecular weight of ~27 kDa in SDS/PAGE.
Molecular Weight 24-27 kDa
Research Area Cancer, Apoptosis/Necrosis
Application Notes Clone A66-2 can be used for western blot analysis (1-2 µg/ml). Other reported applications not routinely tested include immunoprecipitation (1-2 µg/1x10^6 cells). Daudi B lymphoma cells (ATCC CCL-213) are suggested as a positive control.
Comment

Related Products: ABIN967389

Restrictions For Research Use only
Format Liquid
Concentration 0.5 mg/ml
Buffer Aqueous buffered solution.
Preservative Sodium azide
Storage 4 °C
Supplier Images
anti-Fas (TNFRSF6)-Associated Via Death Domain (FADD) antibody Western blot analysis of FADD. Daudi B lymphoma cell lysate was probed with anti-human FADD (clone A66-2) at concentrations of 2.0 (lane 1), 1.0 (lane 2), and 0.5 µg/ml (lane 3). The antibody identifies FADD as an ~27 kDa band.
anti-Fas (TNFRSF6)-Associated Via Death Domain (FADD) antibody (2) anti-Fas (TNFRSF6)-Associated Via Death Domain (FADD) antibody (Image 2)
Product cited in: Cleveland, Ihle: "Contenders in FasL/TNF death signaling." in: Cell, Vol. 81, Issue 4, pp. 479-82, 1995 (PubMed).

Muzio, Chinnaiyan, Kischkel et al.: "FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex." in: Cell, Vol. 85, Issue 6, pp. 817-27, 1996 (PubMed).

Hosts (125), (41), (2)
Reactivities (123), (57), (33), (12), (3), (2), (1)
Applications (116), (76), (40), (36), (24), (17), (8), (6), (2), (2), (2), (1), (1)
Conjugates (4), (4), (4), (4), (4), (4), (4), (4), (4), (4), (4), (4)
Epitopes (30), (25), (13), (8), (6), (3), (3), (2), (1), (1), (1), (1), (1), (1), (1)
Request Want additional data for this product?

The Independent Validation Initiative strives to provide you with high quality data. Find out more

Add to Basket

Order hotline:

  • +1 404 474 4654
  • +1 888 205 9894 (TF)
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