DcR1 peptide (ab5849)
- Product nameDcR1 peptideSee all DcR1 proteins and peptides ...
Our Abpromise guarantee covers the use of ab5849 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
- Purity> 95
% by SDS-PAGE.
- Additional Notes
This peptide may be used for neutralization and control experiments with the polyclonal antibody that reacts with this product and DcR1, catalog ab5808. Using a solution of peptide of equal volume and concentration to the corresponding antibody will yield a large molar excess of peptide (~70-fold) for competitive inhibition of antibody-protein binding reactions.
- Concentration information loading...
Preparation and Storage
- Stability and Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
- Antagonist decoy receptor for TRAIL/Apo 2L
- Cytotoxic TRAIL receptor 3
- DcR 1
- DCR1 TNFR
- Decoy Receptor 1
- Decoy TRAIL receptor without death domain
- Lymphocyte inhibitor of TRAIL
- TNF Related Apoptosis Inducing Ligand Receptor 3
- TNF-re ated apoptosis inducing ligand receptor 3
- TRAIL R3
- TRAIL receptor 3
- TRAIL Receptor Without An Intracellular Domain
- Tumor Necrosis Factor Receptor Superfamily Member 10C
- Tumor necrosis factor receptor superfamily, member 10c, decoy without an intracellular domain
- RelevanceDcR1 / TRAIL-R3 / TRID / LIT is one of the two putative decoy receptors identified for TRAIL, one of the members of TNF family of apoptosis inducing proteins. The other putative decoy receptor is called DcR2 / TRUNDD / TRAIL-R4. DcR1 is attached to the cell surface through glycophospholipid anchor. It has the extracellular TRAIL binding domain but lacks the cytoplasmic domain to induce apoptotic signal. Hence overexpression of DcR1 inhibits the TRAIL induced apoptosis.
- Cellular localizationCell Membrane and Cytoplasmic
References for DcR1 peptide (ab5849)
ab5849 has not yet been referenced specifically in any publications.