|Application ||WB, FC, IP|
|Host||Purified From Concentrated Hybridoma Tissue Culture Supernatant.|
|Application Note||FC,IP,WB,Functional Application, Induces apoptosis with or without cross-linking (Protein A), depending on cell type.|
|Calculated MW||37732 Da|
|Other Names||CD95; APO-1; TNFRSF6; Tumor Necrosis Factor Receptor Superfamily Member 6; Apoptosis-mediating Surface Antigen FAS|
|Target/Specificity||Recognizes human Fas.|
|Format||Liquid. In PBS.|
|Reconstitution & Storage||Stable for at least 1 year after receipt when stored at -20°C.|
|Precautions||Functional Fas (human) Antibody, mAb (preservative free) is for research use only and 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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Provided below are standard protocols that you may find useful for product applications.
Fas (CD95) is a member of the death receptor (DR) family, a subfamily of the tumor necrosis factor receptor superfamily. The formation of the Fas death-inducing signaling complex (DISC) is the initial step of Fas signaling. Activation of procaspase-8 at the DISC leads to the induction of DR-mediated apoptosis. Stimulation of Fas has been also reported to trigger non-apoptotic pathways. It has been shown that membrane-bound FasL is essential for the cytotoxic activity, whereas soluble FasL appears to promote autoimmunity and tumorigenesis via induction of non-apoptotic pathways, in particular NF-kappa.
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