Abstract
Fas (Apo-1 or CD95) and its corresponding ligand FasL (CD95L) are representative members of the TNF receptor and TNF ligand family that have been implicated in a variety of apoptotic processes, involved in T-cell induced cytotoxicity, activation-induced cell death, immune privilege, tumor surveillance and angiogenesis. Although, studies on the FasL/Fas system mainly focused on its pro-apoptotic role, a couple of additional apoptosis-independent functions of Fas have been reported, including induction of proliferation in T-cells and fibroblasts, hepatocyte regeneration, chemokine production, DC maturation and neurite outgrowth. While the apoptotic signaling capacities of FasL and Fas were intensively studied and well understood, the molecular mechanisms of nonapoptotic Fas signaling are ill defined yet. This chapter will review our current understanding of nonapoptotic FasL/Fas functions and in particular address how the balance between apoptotic and nonapoptotic Fas signaling is regulated.
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Wajant, H. (2006). Fas—More Than an Apoptosis Inducer. In: Fas Signaling. Medical Intelligence Unit. Springer, Boston, MA. https://doi.org/10.1007/0-387-34573-6_6
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