| 產(chǎn)品詳情 |
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| Product Name | sFas Ligand ELISA |
| Description | Fas (APO-1, CD95) is a type I membrane protein that belongs to the TNF/nerve growth factor receptor family. Fas mediates apoptosis, the programmed cell death, when it is cross-linked with specific binding partners. The natural binding partner of Fas is its ligand, Fas-L, which is a 37 kDa type II-membrane protein that belongs to the TNF family which includes TNF, lymphotoxin, TNF-related apoptosis-inducing ligand (TRAIL), CD40 ligand, CD27 ligand, CD30 ligand, and OX40 ligand. Fas-L is predominantly expressed on activated T-cells and NK cells, thus Fas-L-mediated cell death is involved in the T or NK cell-mediated cytotoxicity, some pathologic tissue damages, and the regulation of lymphocyte homeostasis. A soluble form of Fas-L (sFas-L) is naturally produced by metalloproteinase- mediated processing. The soluble form resulting from this cleavage was shown to induce apoptosis in susceptible cells. Markedly elevated levels of sFas-L have been shown in TEN (Toxic Epidermal Necrolysis, Lyell's Syndrom) patients' sera. Liver dysfunction was shown to be paralleled by increased sFas-L levels as well as kidney damage. Fas-L is discussed to be involved in the pathogenesis of autoimmune diseases, especially the concentrations of sFas-L are remarkably higher in the sera and synovial fluids of patients with severe rheumatoid arthritis as compared to normal controls. Increased levels of soluble Fas-L in the serum of graft-versus-host disease patients make it a good marker for treatment of the disease. Sample Types: Human cell culture, citrate plasma, EDTA plasma, heparin plasma, serum. Sample Size: 50 μL. Range: 0.16 - 10.0 ng/mL. Sensitivity: 0.07 ng/mL. Time: 3hr 10min |
| Size | 96 wells |
| Concentration | n/a |
| Applications | Immunoassays. Research Use Only. Not for Use in Diagnostic Procedures. |
| Other Names | n/a |
| Gene, Accession, CAS # | n/a |
| Catalog # | 61-FALHU-E01 |
| Price | |
| Order / More Info | sFas Ligand ELISA from ALPCO |
| Product Specific References | n/a |
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