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AdipoGen Life Sciences
anti-TRAIL-R1 (human), mAb (HS101)
460
CHF
CHF 460.00
In stock
AG-20B-0022-C100100 µgCHF 460.00
Product Details | |
---|---|
Synonyms | TRAIL Receptor 1; DR4; APO2; TNFRSF10A; CD261 |
Product Type | Monoclonal Antibody |
Properties | |
Clone | HS101 |
Isotype | Mouse IgG1 |
Source/Host | Purified from concentrated hybridoma tissue culture supernatant. |
Immunogen/Antigen | Recombinant human TRAIL-R1 (DR4). |
Application |
Flow Cytometry |
Crossreactivity | Human |
Specificity |
Recognizes human TRAIL-R1. Does not cross-react with human TRAIL-R2, -R3 or -R4. |
Purity | ≥95% (SDS-PAGE) |
Purity Detail | Protein G-affinity purified. |
Concentration | 1mg/ml |
Formulation | Liquid. In PBS containing 10% glycerol and 0.02% sodium azide. |
Isotype Negative Control | |
Shipping and Handling | |
Shipping | BLUE ICE |
Short Term Storage | +4°C |
Long Term Storage | -20°C |
Handling Advice |
After opening, prepare aliquots and store at -20°C. Avoid freeze/thaw cycles. |
Use/Stability | Stable for at least 1 year after receipt when stored at -20°C. |
Documents | |
MSDS | Download PDF |
Product Specification Sheet | |
Datasheet | Download PDF |
Description
TRAIL-R1 is a receptor for the cytotoxic ligand TRAIL. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. Promotes the activation of NF-κB.
Product References
- Caspase-10 is recruited to and activated at the native TRAIL and CD95 death-inducing signalling complexes in a FADD-dependent manner but can not functionally substitute caspase-8: M.R. Sprick, et al.; EMBO J. 21, 4520 (2002)
- Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Signaling in Activated T Cells Abrogates TRAIL-Induced Apoptosis Upstream of the Mitochondrial Amplification Loop and Caspase-8: T.S. Soderstrom, et al.; J. Immunol. 169, 2851 (2002)
- Proteasome inhibition results in TRAIL sensitization of primary keratinocytes by removing the resistance-mediating block of effector caspase maturation: M. Leverkus, et al.; Mol. Cell. Biol. 23, 777 (2003)
- TNF-Related Apoptosis-Inducing Ligand Mediates Tumoricidal Activity of Human Monocytes Stimulated by Newcastle Disease Virus: B. Washburn, et al.; J. Immunol. 170, 1814 (2003)
- TRAIL regulates normal erythroid maturation through an ERK-dependent pathway: P. Secchiero, et al.; Blood 103, 517 (2004)
- IFN{alpha}-stimulated neutrophils and monocytes release a soluble form of TNF-related apoptosis-inducing ligand (TRAIL/Apo-2 ligand) displaying apoptotic activity on leukemic cells: C. Tecchio, et al.; Blood 103, 3837 (2004)
- Enhanced caspase-8 recruitment to and activation at the DISC is critical for sensitisation of human hepatocellular carcinoma cells to TRAIL-induced apoptosis by chemotherapeutic drugs: T.M. Ganten, et al.; Cell Death Differ. 11 Suppl 1, 86 (2004)
- Casein kinase I attenuates tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by regulating the recruitment of fas-associated death domain and procaspase-8 to the death-inducing signaling complex: K. Izeradjene, et al.; Cancer Res. 64, 8036 (2004)
- cFLIPL inhibits tumor necrosis factor-related apoptosis-inducing ligand-mediated NF-kappaB activation at the death-inducing signaling complex in human keratinocytes: T. Wachter, et al.; J. Biol. Chem. 279, 52824 (2004)
- Resistance to FasL and tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in Sezary syndrome T-cells associated with impaired death receptor and FLICE-inhibitory protein expression: E. Contassot, et al.; Blood 111, 4780 (2008)
- TRAIL-R2-specific antibodies and recombinant TRAIL can synergise to kill cancer cells: M.H. Tuthill, et al.; Oncogene 34, 2138 (2015)
- The TRAIL-Induced Cancer Secretome Promotes a Tumor-Supportive Immune Microenvironment via CCR2: T. Hartwig, et al.; Mol. Cell 65, 730 (2017)
- NCTR25 fusion facilitates the formation of TRAIL polymers that selectively activate TRAIL receptors with higher potency and efficacy than TRAIL: Y. Wang, et al.; Cancer Chemother. Pharmacol. 88, 289 (2021)