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Sci. STKE, 5 August 2003 CONNECTIONS MAP OVERVIEWSThe FasL-Fas Signaling NetworkDepartment of Molecular Internal Medicine, Medical Polyclinic, University of Wuerzburg Roentgenring 11, 97070 Wuerzburg, Germany. stkecm;CMP_7966Abstract: Fas ligand (FasL; also known as APO-1L or CD95L) belongs to the tumor necrosis factor (TNF) ligand family, and its corresponding receptor, Fas (also known as APO-1 or CD95), is a typical member of the death receptor subgroup of the TNF receptor superfamily. Both molecules were originally identified through their apoptosis-inducing capabilities. In recent years, however, roles for Fas and FasL in nonapoptotic processes have become apparent. Fas and FasL have been implicated in such diverse processes as activation-induced cell death (AICD) in T cells, cytotoxic T cell (CTL) function, immune privilege, tumor surveillance, T cell proliferation, dendritic cell differentiation, cardiac hypertrophy, and neurite growth. Many fundamental aspects of the extrinsic apoptotic pathway, including the identification of the death domain, the definition of the death-inducing signaling complex (DISC), the cell type-specific dependency of death receptor induced apoptosis from a mitochondrial amplification loop, and the mechanisms of procaspase activation, were initially identified in the context of Fas-FasL-related studies; thus, this system is a paradigm for apoptotic death receptor signaling. The canonical Fas signaling pathway depicted in the Connections Map provides a comprehensive overview of the molecules and their relations that contribute to the complex signaling network triggered by Fas-FasL interaction. Science Viewpoint H. Wajant, The Fas signaling pathway: More than a paradigm. Science 296, 1635-1636 (2002). [Abstract] [Full Text] *Contact information. Telephone, 49-931-201-71000; fax, 49-931-201-71070; e-mail, harald.wajant{at}mail.uni-wuerzburg.de
Citation: H. Wajant, The FasL-Fas Signaling Network. Sci. STKE 2003, cm5 (2003). |
Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882