Human CD95 ELISA Kit | FAS elisa kit
Human CD95 ELISA Kit
Background/Introduction: Fas, also known as APO-1, CD95 and TNFRSF6, is a member of the nerve growth factor (NGF)/tumour necrosis factor (TNF) receptor superfamily and mediates apoptosis. The nucleotide sequence of the cDNAs reveales that the molecule coding for the Fas antigen determinant is a 319 amino acid polypeptide with a single transmembrane domain. The extracellular domain is rich in cysteine residue, and shows a similarity to that of human tumor necrosis factor receptors, human nerve growth factor receptor, and human B cell antigen CD40. The APO-1 antigen as defined by the mouse monoclonal antibody anti-APO-1 is previously found to be expressed on the cell surface of activated human T and B lymphocytes and a variety of malignant human lymphoid cell lines. The APO-1 antigen is found to be a membrane glycoprotein of 48 kDa. Fas antigen is expressed and functional on papillary thyroid cancer cells and this may have potential therapeutic significance. Fas can play a role as an inducer of both neurite growth in vitro and accelerates recovery after nerve injury in vivo. The FAS and FASL triggered apoptosis pathway plays an important role in human carcinogenesis.
NCBI and Uniprot Product Information
NCBI Description
The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor contains a death domain. It has been shown to play a central role in the physiological regulation of programmed cell death, and has been implicated in the pathogenesis of various malignancies and diseases of the immune system. The interaction of this receptor with its ligand allows the formation of a death-inducing signaling complex that includes Fas-associated death domain protein (FADD), caspase 8, and caspase 10. The autoproteolytic processing of the caspases in the complex triggers a downstream caspase cascade, and leads to apoptosis. This receptor has been also shown to activate NF-kappaB, MAPK3/ERK1, and MAPK8/JNK, and is found to be involved in transducing the proliferating signals in normal diploid fibroblast and T cells. Several alternatively spliced transcript variants have been described, some of which are candidates for nonsense-mediated mRNA decay (NMD). The isoforms lacking the transmembrane domain may negatively regulate the apoptosis mediated by the full length isoform. [provided by RefSeq, Mar 2011]
Uniprot Description
FAS: 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). Binds DAXX. Interacts with HIPK3. Part of a complex containing HIPK3 and FADD. Binds RIPK1 and FAIM2. Interacts with BRE and FEM1B. Interacts with FADD. 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. 6 isoforms of the human protein are produced by alternative splicing.
Protein type: Membrane protein, integral; Cell surface; Apoptosis; Receptor, cytokine
Chromosomal Location of Human Ortholog: 10q24.1
Cellular Component: apical plasma membrane; CD95 death-inducing signaling complex; cell soma; cell surface; cytoplasm; cytosol; external side of plasma membrane; extracellular space; integral to plasma membrane; lipid raft; neuron projection; nucleus; perinuclear region of cytoplasm; plasma membrane; sarcolemma; secretory granule
Molecular Function: identical protein binding; kinase binding; protease binding; protein binding; protein complex binding; receptor activity; signal transducer activity; tumor necrosis factor receptor activity
Biological Process: activated T cell apoptosis; aging; apoptosis; B cell mediated immunity; brain development; caspase activation; cell surface receptor linked signal transduction; chordate embryonic development; circadian rhythm; dendrite regeneration; immune response; immunoglobulin production; induction of apoptosis via death domain receptors; inflammatory cell apoptosis; inflammatory response; maternal process involved in pregnancy; negative regulation of apoptosis; negative regulation of B cell activation; negative regulation of caspase activity; negative thymic T cell selection; ovarian follicle atresia; ovulation cycle; positive regulation of apoptosis; positive regulation of MAPKKK cascade; positive regulation of protein homooligomerization; programmed cell death; protein complex assembly; protein homooligomerization; regulation of apoptosis; regulation of caspase activity; regulation of cell proliferation; regulation of gene expression; regulation of lymphocyte differentiation; regulation of myeloid cell differentiation; renal system process; response to cycloheximide; response to drug; response to glucocorticoid stimulus; response to lipopolysaccharide; response to peptide hormone stimulus; response to toxin; signal transduction; spermatogenesis; spleen development; telencephalon development; transformed cell apoptosis; tumor necrosis factor-mediated signaling pathway
Disease: Autoimmune Lymphoproliferative Syndrome