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小鼠凋亡相关因子配体(FASL)酶联免疫吸附试剂盒
Catalog #: E03F0051
Sample Type: Biological samples
BackgroundDatasheetStandard CurveProtocol DownloadsFAQs

 

Other Names

Mouse FAS Ligand ELISA kit

FASL; CD178; CD95L; CD95-L; FASLG; FASLG; APT1LG1; APT1-LG1; TNFSF6; Fas Antigen Ligand; TNF Superfamily Member 6; Tumor Necrosis Factor(ligand)Superfamily,Member 6

Research Area

Cell Biology, Immunology, Stem Cells

Background

FasL, the physiological agonist for Fas, is also a transmembrane protein with homology to the TNF family in its extracellular domain. FasL is expressed primarily by activated T lymphocytes and by cells of the small intestine and lung. Mice with mutations in either Fas or FasL exhibit accumulation of activated lymphocytes and classical autoimmune symptoms, suggesting that a major function of Fas-mediated apoptosis is the elimination of activated immune cells from the peripheral circulation. Similarly, humans with autoimmune lymphoproliferative syndrome have mutations in Fas. Fas and FasL have been observed as soluble molecules in addition to their membraneassociated forms, suggesting additional complexity to regulation of this apoptotic mechanism. Soluble Fas (sFas) arises from alternatively spliced mRNA, leading to proteins with deletion or disruption of the single membrane-spanning domain. Five alternatively spliced Fas mRNAs have been described, each protein detected in the supernate of cultures of peripheral blood mononuclear cells or certain tumor cell lines. Each sFas inhibited apoptosis induced by FasL, and tumor-cell lines resistant to anti-Fas were shown to produce alternatively spliced Fas, thereby making them less sensitive to FasL. In addition, plasma Fas can arise by exfoliation of membrane vesicles, which also inhibit FasL-induced apoptosis. Serum Fas has been reported to be elevated in cancer patients , possibly originating in the tumor cell itself), and in autoimmune diseases .