TNFR1 (Tumor Necrosis Factor Receptor Superfamily Member 1A, Tumor Necrosis Factor Receptor 1, p55, p60, TNF-R1, Tumor Necrosis Factor Receptor Type I, TNF-RI, TNFR-I, p55, CD120a, Tnfrsf1a, Tnfr-1) (FITC)

TNF-RI belongs to the large TNF receptor family, among which TNF-RII (TNF-R p75-80), lymphotoxin-beta receptor (LTbetaR) and the Herpes virus entry mediator (HVEM). Ligands for these receptors belong to the Tumor Necrosis Factor (TNF) superfamily of cytokines, which activate signaling pathways for cell survival, death, and differentiation that orchestrate the development, organization and homeostasis of lymphoid, mammary, neuronal and ectodermal tissues. TNF-RI contains a characteristic structural cassette termed death domain in its sequence that is conserved within a distinct subset of other TNF-R family members, such as CD95, DR3, DR4, and DR5. This death domain, was characterized as being essential for induction of apoptosis in vitro and has been structurally conserved within these TNF-R superfamily members. Deletion of the death domain of the TNF-RI results in a non-functional receptor, indicating that the death domain is required for the signal transduction of the physiological functions of TNF-RI in vivo. TNF-RI is a 55kD type I transmembrane protein and is expressed on a variety of cell types at low levels. It is considered to play a prominent role in cell stimulation by TNF-alpha. Induction of cytotoxicity and other functions are mediated largely via TNF-RI. TNF-RI is present as soluble form in body fluids (for instance plasma and CSF). This extracellular TNF-RI is generated by two mechanisms, namely proteolytic cleavage of TNF-RI ectodomains and release of full-length TNF-RI in the membranes of exosome-like vesicles. TNF-RI and TNF-RII both interact with the homomeric forms of LTbeta or TNF. However, TNF-RI functions as the high affinity receptor for soluble TNF (sTNF). TNF-RI has been shown to be involved in a wide variety of inflammatory diseases, among which neurodegenerative diseases (Parkinson's and Alzheimer's disease), multiple sclerosis, asthma, atherosclerosis, rheumatology.\n\nApplications:\nSuitable for use in Flow Cytometry, ELISA, Functional Assays and Immunoprecipitation. Other applications not tested.\n\nRecommended Dilution:\nFlow Cytometry: 1:50\nFunctional Assays: This monoclonal antibody is an antagonistic antibody useful for blocking of TNR-RI both in vitro.\nOptimal dilutions to be determined by the researcher.\n\nStorage and Stability:\nMay be stored at 4 degrees C for short-term only. For long-term storage and to avoid repeated freezing and thawing, aliquot and store at -20 degrees C. Aliquots are stable for 12 months at -20 degrees C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer. FITC conjugates are sensitive to light.

Prices direct from United States Biological

Quick response times

Exclusive Biosave savings/discounts

SPECIFICATIONS

Catalog Number

T9161-19E

Size

100ug

Applications

ELISA, FC, IP

Reactivities

Mouse

Form

Supplied as a liquid in PBS, 1% BSA, 0.02% sodium azide. Labeled with fluorescein isothiocyanate (FITC).

P Type

Mab

Purity

Purified by Protein G affinity chromatography.

Isotype

IgG1

References

1. Sheehan, K et al; Monoclonal antibodies specific for murine p55 and p75 tumor necrosis factor receptors: identification of a novel in vivo role for p75. J Exp Med 1995, 181: 607. 2. Pinckard, J et al; Ligand-induced formation of p55 and p75 tumor necrosis factor receptor heterocomplexes on intact cells. J Biol Chem 1997, 272: 10784. 3. Ji, H et al; Critical roles for interleuking 1 and tumor necrosis factor alpha in antibody-induced arthritis. J Exp Med 2002, 196: 77. 4. Lee, S et al; Inhibition of TCR-induced CD8 T cell death by IL-12: regulation of Fas ligand and cellular FLIP expression and caspase activation by IL-12. J Immunol 2003, 170: 2456.

Additional Info

Recognizes the extracellular part of mouse TNF-RI.