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Specifications
- Protein/Peptide Type:Recombinant
- Source:HEK293 cells
- Species:Human
- Size:0.1 mg
- Environmentally Preferable:
- Tag sequence:C-Fc Tag
- Biological Activity:Measured by its binding ability in a functional ELISA. Immobilized Human Fas Ligand, His Tag at 5ug/mL (100 uL/well) can bind Human Fas, Fc Tag with a linear range of 1.56-12.5 ng/mL.
- Protein Synonyms:FasR|FAS|FASTM|APO1|ALPS1A|TNFRSF6|CD95|APT1|FAS1
- Protein/Peptide Name:CD95
- Purity:>95% as determined by SDS-PAGE.
- Molecular Weight:42.8 kDa
- Formulation:Lyophilized, 50 mM tris, 100 mM glycine, pH7.5
- Tested Applications:Western Blot
- Cat. No.:10798-180
- Supplier no.:96-302
Specifications
About this item
The Fas is also known as FAS receptor (FasR), apoptosis antigen 1 (APO-1 or APT), cluster of differentiation 95 (CD95) or tumor necrosis factor receptor superfamily member 6 (TNFRSF6). is a death receptor on the surface of cells that leads to programmed cell death (apoptosis). It is one of two apoptosis pathways, the other being the mitochondrial pathway. FasR is located on chromosome 10 in humans and 19 in mice. Similar sequences related by evolution (orthologs) are found in most mammals. Fas forms the death-inducing signaling complex (DISC) upon ligand binding. Membrane-anchored Fas ligand trimer on the surface of an adjacent cell causes trimerization of Fas receptor. This event is also mimicked by binding of an agonistic Fas antibody, though some evidence suggests that the apoptotic signal induced by the antibody is unreliable in the study of Fas signaling. To this end, several clever ways of trimerizing the antibody for in vitro research have been employed.Upon ensuing death domain (DD) aggregation, the receptor complex is internalized via the cellular endosomal machinery. This allows the adaptor molecule FADD to bind the death domain of Fas through its own death domain. Recently, Fas has also been shown to promote tumor growth, since during tumor progression, it is frequently downregulated or cells are rendered apoptosis resistant. Cancer cells in general, regardless of their Fas apoptosis sensitivity, depend on constitutive activity of Fas. This is stimulated by cancer-produced Fas ligand for optimal growth.