|Other Names||Tumor necrosis factor receptor superfamily member 6, Apo-1 antigen, Apoptosis-mediating surface antigen FAS, FASLG receptor, CD95, FAS, APT1, FAS1, TNFRSF6|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Synonyms||APT1, FAS1, TNFRSF6|
|Function||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).|
|Cellular Location||Isoform 1: Cell membrane; Single-pass type I membrane protein Isoform 3: Secreted. Isoform 5: Secreted.|
|Tissue Location||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.|
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The protein encoded by this gene is a member of theTNF-receptor superfamily. This receptor contains a death domain. Ithas been shown to play a central role in the physiologicalregulation of programmed cell death, and has been implicated in thepathogenesis of various malignancies and diseases of the immunesystem. The interaction of this receptor with its ligand allows theformation of a death-inducing signaling complex that includesFas-associated death domain protein (FADD), caspase 8, and caspase10. The autoproteolytic processing of the caspases in the complextriggers a downstream caspase cascade, and leads to apoptosis. Thisreceptor has been also shown to activate NF-kappaB, MAPK3/ERK1, andMAPK8/JNK, and is found to be involved in transducing theproliferating signals in normal diploid fibroblast and T cells. Atleast eight alternatively spliced transcript variants have beendescribed, some of which are candidates for nonsense-mediated decay(NMD). The isoforms lacking the transmembrane domain may negativelyregulate the apoptosis mediated by the full length isoform.
Cao, Y., et al. Mol. Carcinog. 49(11):944-950(2010)Glavan, B.J., et al. Am. J. Respir. Crit. Care Med. (2010) In press :Gizinger, O.A., et al. Vopr Kurortol Fizioter Lech Fiz Kult 3, 29-31 (2010) :Dubikov, A.I., et al. Scand. J. Rheumatol. 39(5):368-372(2010)Chakrabandhu, K., et al. EMBO J. 26(1):209-220(2007)
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