- Catalogue N°
- 850.740.048 - 1 x 48 Discovery (pre-coated)
850.740.096 - 1 x 96 (pre-coated)
850.740.192 - 2 x 96 (pre-coated)
- Assay Range
- 93.75 pg/ml - 3000 pg/ml
- 47 pg/ml
- Target species
- Recognizes both natural and recombinant soluble human Fas
- Sample Type
- Serum, Plasma, Cell culture supernatant
- Sample Size
- 100 µl
- Cross Reaction
- No cross reactivity with other human soluble molecules
- Kit Content
- Diaclone ELISA Kits include pre-coated strip plates, biotinylated secondary antibody, standards, controls (where applicable), buffers, streptavidin-HRP, TMB, stop reagents and a detailed procedure.
Fas (APO-1, CD95) is a transmembrane protein belonging to the TNF receptor family, capable of mediating apoptotic death of transformed cells as well as activated human T cells. The cell death signal can be induced by anti-Fas antibodies or by the Fas (Fas-L) ligand belonging to the TNF family. The in vivo expression of these two Fas and Fas-L molecules is differently regulated since the expression of Fas is pleiotropic whereas Fas-L is rather expressed in immunity sites (testes, ovaries, brain, eye) and by activated T cells. Tumor cells regardless of their tissue origin may also express Fas-L (pathological).
Genetic and immunological studies have shown that the Fas system is on the one hand involved in the process of peripheral clonal deletion allowing the maintenance of self-tolerance, on the other hand that it regulates the amplitude and duration of immune responses. and finally that it represents one of the mechanisms of lysis of the target cells in the antiviral cytotoxic T response.
When Fas-dependent apoptosis can not occur, due to genetic mutations in the Fas or Fas-L genes, a lymphoproliferative syndrome and autoimmune manifestations are observed in humans and mice. Conversely, an exacerbation of the Fas system may be responsible for tissue destruction. For example, the single mouse injection of anti-Fas antibodies induces massive liver destruction and mouse death within a few hours, leading to the hypothesis of Fas involvement in fulminant hepatitis.
Version 13 - 02.20
For research use only
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