Cross reactivity: Mouse TNF-RI : Yes, Mouse TNF-alpha Minimal crossreactivity problematic in case of TNF-RII knockout studies and when used in high concentrations in functional studies
TNFRSF1B
Reactivity: Rat
WB, IHC, ICC
Host: Rabbit
Polyclonal
unconjugated
Application Notes
For flow cytometry and Western blotting, dilutions to be used depend on detection system applied. It is recommended that users test the reagent and determine their own optimal dilutions. The typical starting working dilution is 1:50. For functional studies, in vitro dilutions have to be optimized in user's experimental setting.
Restrictions
For Research Use only
Buffer
PBS, containing 0.1 % bovine serum albumin
Storage
4 °C
Storage Comment
Product should be stored at 4 °C. Under recommended storage conditions, product is stable for one year.
Expiry Date
12 months
Gerspach, Götz, Zimmermann, Kolle, Böttinger, Grell: "Detection of membrane-bound tumor necrosis factor (TNF): an analysis of TNF-specific reagents." in: Microscopy research and technique, Vol. 50, Issue 3, pp. 243-50, (2000) (PubMed).
Lucas, Garcia, Donati, Hribar, Mandriota, Giroud, Buurman, Fransen, Suter, Nunez, Pepper, Grau: "Both TNF receptors are required for direct TNF-mediated cytotoxicity in microvascular endothelial cells." in: European journal of immunology, Vol. 28, Issue 11, pp. 3577-86, (1998) (PubMed).
Bemelmans, Gouma, Buurman: "LPS-induced sTNF-receptor release in vivo in a murine model. Investigation of the role of tumor necrosis factor, IL-1, leukemia inhibiting factor, and IFN-gamma." in: Journal of immunology (Baltimore, Md. : 1950), Vol. 151, Issue 10, pp. 5554-62, (1993) (PubMed).
Target
TNFRSF1B
(Tumor Necrosis Factor Receptor Superfamily, Member 1B (TNFRSF1B))
The polyclonal antibody recognizes the extracellular part of the mouse Tumor Necrosis Factor Receptor type 2 (TNF-RII) of the membrane-bound as well as the soluble receptor. TNF-RII (~75-80 kDa) is present on most cell types and is considered to play a prominent role in cell stimulation by TNF-alpha. TNF-alpha activates inflammatory responses, induces apoptosis, regulates cellular proliferation, and may even promote cancer progression. The effects of TNF-alpha are mediated by TNF-RI and TNF-RII, which have both distinct and overlapping downstream signaling cascades. Induction of cytotoxicity and other functions are mediated largely via TNF-RI. TNF-RI is equally well activated by both the 17 kDa soluble and 26 kDa membrane-bound form, whereas TNF-RII is efficiently activated only by the membrane bound form of TNF-alpha. Binding of the inherently trimeric TNF-alpha to TNFR1 and TNFR2 induces receptor trimerization and recruitment of several signaling proteins to the cytoplasmic domains of the receptors. Occupancy of TNFR2 results in direct recruitment of TNF Receptor Associated Factor 2 (TRAF2), which in turn recruits TRAF1. Aliases Tumor necrosis factor receptor superfamily member 1B, TNF-RII, p75/p80