The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
IHC-P: Use neat for 10 minutes at room temperature. Antigen retrieval is not essential but boiling tissue sections in 10mM citrate buffer, pH 6.0 for 10-20 minutes followed by cooling at RT for 20 minutes may optimise staining.
Not yet tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
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.
Involvement in disease
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.