Upstream / Downstream

pathwayImage

Explore pathways related to this product.

Antibody Guarantee

CST Antibody Performance Guarantee

LEARN MORE  

To get local purchase information on this product, click here

Questions?

Find answers on our FAQs page.

ANSWERS  

Visit PhosphoSitePlus®

PTM information and tools available.

LEARN MORE

Product Includes Quantity Applications Reactivity MW(kDa) Isotype
Fas (C18C12) Rabbit mAb 4233 40 µl
Western Blotting Immunohistochemistry
H 40-50 Rabbit IgG
TNF-R1 (C25C1) Rabbit mAb 3736 40 µl
Western Blotting Immunoprecipitation
H 55 Rabbit IgG
TNF-R2 Antibody 3727 40 µl
Western Blotting Immunoprecipitation
H M R 65 Rabbit 
DR5 (D4E9) XP® Rabbit mAb 8074 40 µl
Western Blotting Immunoprecipitation Immunofluorescence
H 40, 48 Rabbit IgG
DcR2 (D13H4) Rabbit mAb 8049 40 µl
Western Blotting Immunoprecipitation
H Mk 45-60 Rabbit IgG
DcR3 Antibody 4758 40 µl
Western Blotting
H R 32 Rabbit 
FADD Antibody (Human Specific) 2782 40 µl
Western Blotting
H 28 Rabbit 
TRADD (7G8) Rabbit mAb 3684 40 µl
Western Blotting Immunoprecipitation
H 32 Rabbit IgG
RIP (D94C12) XP® Rabbit mAb 3493 40 µl
Western Blotting Immunoprecipitation Immunofluorescence Flow Cytometry
H M R Hm Mk 78 Rabbit IgG
Anti-rabbit IgG, HRP-linked Antibody 7074 100 µl
Western Blotting
All Goat 

Product Description

The Death Receptor Antibody Sampler Kit provides an economical means to investigate the machinery of death receptor-mediated apoptosis. The kit includes enough of each primary antibody to perform four western mini-blot experiments per primary.


Specificity / Sensitivity

Each antibody in the Death Receptor Antibody Sampler Kit recognizes endogenous levels of the respective target protein. The TNF-R1, DR5, and RIP antibodies do not cross-react with other related family members. TNF-R1 (C25C1) Rabbit mAb may recognize a 30 kDa splice isoform of TNF-R1 in some cell lines.


Source / Purification

Monoclonal antibodies are produced by immunizing animals with synthetic peptides corresponding to residues surrounding Lys259 of human Fas protein, Ser331 of human TNF-R1 protein, Arg260 of human DR5 protein, Gly227 of human TRADD protein, Leu190 of human RIP protein, or Gly270 of human DcR2 protein.

Polyclonal antibodies are produced by immunizing animals with synthetic peptides corresponding to residues surrounding Asp335 of human TNF-R2 protein, Ser194 of human FADD protein, or near the amino terminus of human DcR3 protein. Polyclonal antibodies are purified by protein A and peptide affinity chromatography.

The tumor necrosis factor receptor family, which includes TNF-RI, Fas, DR3, DR4, DR5, and DR6, plays an important role in the regulation of apoptosis in various physiological systems (1,2). The receptors are activated by a family of cytokines that include TNF, FasL, and TRAIL. They are characterized by a highly conserved extracellular region containing cysteine-rich repeats and a conserved intracellular region of about 80 amino acids termed the death domain (DD). The DD is important for transducing the death signal by recruiting other DD containing adaptor proteins (FADD, TRADD, RIP) to the death-inducing signaling complex (DISC) resulting in activation of caspases. Death receptor signaling is also controlled by a family of decoy receptors (DcR1, DcR2, and DcR3) which lack a cytoplasmic DD and inhibit death receptor-mediated apoptosis by competing for ligand (3-5). The RIP (receptor-interacting protein) family of serine-threonine kinases (RIP, RIP2, RIP3, and RIP4) are important regulators of cellular stress that can trigger pro-survival and inflammatory responses through the activation of NF-κB as well as pro-apoptotic pathways (6). In addition to the kinase domain, RIP contains a death domain responsible for interaction with the death domain receptor Fas and for the recruitment to TNFR1 through interaction with TRADD (6,7). Overexpression of RIP induces both NF-κB activation and apoptosis (7,8). Caspase-8 dependent cleavage of the death domain on RIP can trigger the apoptotic activity of RIP (9). RIP-deficient cells show a failure in TNF-mediated NF-κB activation, making the cells more sensitive to apoptosis (10,11).


1.  Meylan, E. and Tschopp, J. (2005) Trends Biochem Sci 30, 151-9.

2.  Thorburn, A. (2004) Cell Signal 16, 139-44.

3.  Hsu, H. et al. (1996) Immunity 4, 387-96.

4.  Nagata, S. (1997) Cell 88, 355-65.

5.  Sheridan, J.P. et al. (1997) Science 277, 818-21.

6.  Stanger, B.Z. et al. (1995) Cell 81, 513-23.

7.  Marsters, S.A. et al. (1997) Curr Biol 7, 1003-6.

8.  Ting, A.T. et al. (1996) EMBO J 15, 6189-96.

9.  Pitti, R.M. et al. (1998) Nature 396, 699-703.

10.  Kelliher, M.A. et al. (1998) Immunity 8, 297-303.

11.  Lin, Y. et al. (1999) Genes Dev 13, 2514-26.


Entrez-Gene Id 8793
Swiss-Prot Acc. Q9UBN6


For Research Use Only. Not For Use In Diagnostic Procedures.
Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.
U.S. Patent No. 5,675,063.