The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use 0.25µg for 105-8 cells.
Receptor for TNFSF6/FASLG. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both. The secreted isoforms 2 to 6 block apoptosis (in vitro).
Isoform 1 and isoform 6 are expressed at equal levels in resting peripheral blood mononuclear cells. After activation there is an increase in isoform 1 and decrease in the levels of isoform 6.
Defects in FAS are the cause of autoimmune lymphoproliferative syndrome type 1A (ALPS1A) [MIM:601859]; also known as Canale-Smith syndrome (CSS). ALPS is a childhood syndrome involving hemolytic anemia and thrombocytopenia with massive lymphadenopathy and splenomegaly.
Contains 1 death domain. Contains 3 TNFR-Cys repeats.
Contains a death domain involved in the binding of FADD, and maybe to other cytosolic adapter proteins.
Staining of mouse CD95 transfected L5178Y cells with 0.125 µg of Biotin conjugated Armenian Hamster IgG Isotype Control (open histogram) or ab95640 at 0.125 µg (filled histogram) followed by Streptavidin PE. Total viable cells were used for analysis.