CD95 (APO-1/Fas) is an important inducer of the extrinsic apoptosis signaling pathway and therapy induced apoptosis of many tumor cells has been linked to the activity of CD95. is a prototype death receptor characterized by the presence of an 80 amino acid death domain in its cytoplasmic tail. This domain is essential for the recruitment of a number of signaling components upon activation by either agonistic anti-CD95 antibodies or cognate CD95 ligand that initiate apoptosis. The complex of proteins that forms upon triggering of CD95 is called the death-inducting signaling complex (DISC). The DISC consists of an adaptor protein and initiator caspases and is essential for induction of apoptosis. CD95 is also crucial for the negative selection of B cells within the germinal center (GC). Impairment of CD95-mediated apoptosis results in defective affinity maturation and the persistence of autoreactive B-cell clones. Changes in the expression of CD95 and/or its ligand CD95L are frequently found in human cancer. The downregulation or mutation of CD95 has been proposed as a mechanism by which cancer cells avoid destruction by the immune system through reduced apoptosis sensitivity. Thus, CD95 has therefore been viewed as a tumor suppressor. CD95 has been reported to be involved in the activation of NF-kappaB, MAPK3/ERK1, MAPK8/JNK, and the alternate pathways for CTL-mediated cytotoxicity. Accordingly, this protein is implicated in the pathogenesis of various malignancies and diseases of the immune system. The CD95/CD95L system was implicated in the etiology of inflammatory bowel disease (IBD) based, primarily, on the finding that CD95 is highly expressed in the intestinal epithelial cells and that epithelial apoptosis is increased in IBD.
FAS(TNFRSF6) is a receptor and contains three TNFR-Cys repeats and one death domain. It has been shown that FAS is involved in the physiological regulation of programmed cell death, and has been implicated in the pathogenesis of various malignancies and diseases of the immune system. FADD (adapter molecule) 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 mediating apoptosis. FAS-mediated apoptosis may play a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both.
FASN (Fatty Acid Synthase, also FAS) is a cytosolic 270-280 kDa member of the short chain dehydrogenase/reductase family 27X. It is expressed in neurons, skeletal muscle, adipocytes and hepatocytes, and both catalyzes the formation of palmitic acid from acetylCoA and malonylCoA, and likely mediates the transfer of fatty acids to peptides. Human FASN is 2511 amino acids (aa) in length ands contains multiple domains, including a beta-ketoacyl synthase domain (aa 1-414), an acyl and malonyl transferase domain (aa 429-817), an enoyl reductase domain (aa 1563-1863), a beta-ketoacyl reductase domain (aa 1864-2118) and a thioesterase domain (aa 2207-2511). FASN exists as an antiparallel homodimer. There is one theoretical alternative start site at Met2073. Over aa 9-212, human FASN shares 92% aa identity with mouse FASN.
This gene encodes an extracellular matrix protein, which belongs to the fibulin family. This protein binds various extracellular ligands and calcium. It may play a role during organ development, in particular, during the differentiation of heart, skeletal and neuronal structures. Alternatively spliced transcript variants encoding different isoforms have been identified.
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