BioAim Scientific (Kanada)
The Bioaim Mouse TWEAK R ELISA kit is a solid phase sandwich ELISA (enzyme-linked immunosorbent assay) for the quantitative measurement of TWEAK R in mouse serum, plasma and cell culture media. An antibody specific for mouse TWEAK R was coated on a 96-well plate. Standards and samples are added to the wells and any TWEAK R present binds to the immobilized antibody. The wells are washed and biotinylated anti-mouse TWEAK R antibody is added. After washing away unbound biotinylated antibody, HRP-conjugated streptavidin is added to the wells. The wells are again washed and TMB substrate solution is added, which produces a blue color in direct proportion to the amount of TWEAK R present in the initial sample. The Stop Solution changes the color from blue to yellow, and the microwell absorbances are read at 450 nm.Research Area Apoptosis; Osteoclast differentiation;
tumor necrosis factor receptor superfamily, member 12a(TWEAK R) Background: The gene for TNF-related Weak Inducer of Apoptosis Receptor (TWEAK R) was originally identified as the fibroblast growth factor-inducible immediate-early response gene Fn14 in mouse NIH 3T3 fibroblasts. TWEAK R is the smallest member of the TNF receptor superfamily. TWEAK was discovered in 1997.The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is a ligand for the FN14/TWEAKR receptor. This cytokine has overlapping signaling functions with TNF, but displays a much wider tissue distribution. Leukocytes are the main source of TWEAK including human resting and activated monocytes, dendritic cells and natural killer cells. TWEAK can induce apoptosis via multiple pathways of cell death in a cell type-specific manner. This cytokine is also found to promote proliferation and migration of endothelial cells, and thus acts as a regulator of angiogenesis. Excessive activation of the TWEAK pathway in chronic injury has been described to promote pathological tissue changes including chronic inflammation, fibrosis and angiogenesis. In chronic liver disease for example TWEAK expression is enhanced and causes hepatic stellate cells, which are key regulators of liver fibrosis, to proliferate. A disease-driving role of the TWEAK pathway has been described in several other diseases as well. For example, NFAT1 regulates the expression of TWEAKR and its ligand TWEAK (this protein) with lipocalin 2 to increase breast cancer cell invasion.
AI255180, C87282, Fn14, HPIP,TWEAK-R, TweakR
Serum, plasma, Cell culture supernatant
|Antigen Name||tumor necrosis factor receptor superfamily, member 12a|
|Detection Range||102.4-25000 pg/ml|
|Alias||AI255180, C87282, Fn14, HPIP,TWEAK-R, TweakR|