Anti-Fas Antibody Picoband® Fluoro488 Conjugated

FAS (also known as surface antigen APO1 or CD95) is a member of the tumour-necrosis receptor factor family of death receptors. It acts as an inducer of both neurite growth in vitro and accelerated recovery after nerve injury in vivo. FAS antigen is expressed and functional on papillary thyroid cancer cells and this may have potential therapeutic significance. The FAS antigen shows structural homology with a number of cell surface receptors, including tumor necrosis factor (TNF) receptors and the low-affinity nerve growth factor receptor (NGFR) and it is mapped to 10q24.1. The FAS and FASL system plays a key role in regulating apoptotic cell death and corruption of this signalling pathway has been shown to participate in immune escape and tumorigenesis.

Tumor necrosis factor receptor superfamily member 6; Apo-1 antigen; Apoptosis-mediating surface antigen FAS; FASLG receptor; CD95; FAS; APT1, FAS1, TNFRSF6

E.coli-derived human Fas recombinant protein (Position: Q26-N173) . Human Fas shares 55% and 59% amino acid (aa) sequences identity with mouse and rat Fas, respectively.

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. .

Adaptive Immunity, Apoptosis, Autoimmune, Cell Biology, Cytokines, Hematopoietic Progenitors, Immune System Diseases, Immunology, Innate Immunity, Lymphoid, Stem Cells, T Lymphocytic Lineage, TNF Superfamily

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) . .

1. Desbarats, J.; Birge, R. B.; Mimouni-Rongy, M.; Weinstein, D. E.; Palerme, J.-S.; Newell, M. K. : Fas engagement induces neurite growth through ERK activation and p35 upregulation. Nature Cell Biol. 5: 118-125, 2003. 2. Arscott, P. L.; Stokes, T.; Myc, A.; Giordano, T. J.; Thompson, N. W.; Baker, J. R., Jr. : Fas (CD95) expression is up-regulated on papillary thyroid carcinoma. J. Clin. Endocr. Metab. 84: 4246-4252, 1999. 3. Zhang, X.; Miao, X.; Sun, T.; Tan, W.; Qu, S.; Xiong, P.; Zhou, Y.; Lin, D. : Functional polymorphisms in cell death pathway genes FAS and FASL contribute to the risk of lung cancer. J. Med. Genet. 42: 479-484, 2005.