R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
TNF-R1 (D3I7K) Rabbit mAb #13377
Filter:
- WB
Supporting Data
REACTIVITY | M R |
SENSITIVITY | Endogenous |
MW (kDa) | 55 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- M-Mouse
- R-Rat
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
TNF-R1 (D3I7K) Rabbit mAb recognizes endogenous levels of total mouse TNF-R1 protein.
Species Reactivity:
Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of mouse TNF-R1 protein.
Background
TNF-α is an important cytokine produced by numerous cell types, including neutrophils, activated lymphocytes, macrophages, and NK cells. It plays a critical role in inflammatory responses and apoptosis (1). TNF-α exists as a membrane-anchored and soluble form, both of which show biological activity. Response to TNF-α is mediated through two receptors, TNF-R1, which is widely expressed, and TNF-R2, which is expressed mainly in immune and endothelial cells (2). Antagonists to TNF-α have been validated as therapeutic targets for rheumatoid arthritis and other immune disorders (3).
The two receptors for TNF-α, TNF-R1 (55 kDa) and TNF-R2 (75 kDa) can mediate distinct cellular responses (4,5). In most cases cytotoxicity elicited by TNF has been reported to act through TNF-R1 (6,7). Cytotoxicity is mediated by a "death domain" with the intracellular region of the receptor that binds to the death domain adaptor protein TRADD and triggers the activation of caspases (8). Soluble forms of both receptors have also been characterized which can bind TNF-α and may play an important role in immune disorders (9,10).
The two receptors for TNF-α, TNF-R1 (55 kDa) and TNF-R2 (75 kDa) can mediate distinct cellular responses (4,5). In most cases cytotoxicity elicited by TNF has been reported to act through TNF-R1 (6,7). Cytotoxicity is mediated by a "death domain" with the intracellular region of the receptor that binds to the death domain adaptor protein TRADD and triggers the activation of caspases (8). Soluble forms of both receptors have also been characterized which can bind TNF-α and may play an important role in immune disorders (9,10).
- Aggarwal, B.B. (2003) Nat Rev Immunol 3, 745-56.
- Locksley, R.M. et al. (2001) Cell 104, 487-501.
- Taylor, P.C. et al. (2004) Curr Opin Biotechnol 15, 557-63.
- Tartaglia, L.A. et al. (1991) Proc Natl Acad Sci U S A 88, 9292-6.
- Peschon, J.J. et al. (1998) J Immunol 160, 943-52.
- Tartaglia, L.A. et al. (1993) Cell 73, 213-6.
- Rothe, J. et al. (1993) Nature 364, 798-802.
- Chen, G. and Goeddel, D.V. (2002) Science 296, 1634-5.
- Humbert, M. et al. (1994) Am J Respir Crit Care Med 149, 1681-5.
- Schröder, J. et al. (1995) Infection 23, 143-8.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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