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Fas

Domain

Contains a death domain involved in the binding of FADD, and maybe to other cytosolic adapter proteins.

Function

Receptor for TNFSF6/FASLG. The adapter molecule FADD recruits caspase CASP8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs CASP8 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 (By similarity).

Involvement in disease

Defects in Fas are the cause of the lymphoproliferation phenotype (lpr) (PubMed:1372394). Lpr mice show lymphadenopathy and autoantibody production (PubMed:1372394).

Post-translational modifications

Palmitoylated. Palmitoylation by ZDHHC7 prevents the lysosomal degradation of FAS regulating its expression at the plasma membrane.

Tissue Specificity

Detected in various tissues including thymus, liver, lung, heart, and adult ovary.

Cellular localization

Alternative names

CD95, Apt1, Tnfrsf6, Fas, Tumor necrosis factor receptor superfamily member 6, Apo-1 antigen, Apoptosis-mediating surface antigen FAS, FASLG receptor

swissprot:P25446 entrezGene:14102

Other research areas