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Abstract A variety of biological functions are regulated through extracellular signals. Amongst the best studied examples is growth control, which is achieved by the regulatory function of glrOwthfactors,. Proqrammed cell death (apoptcsis) is controlled in a similar fashion. Apoptosis, firstly a morphologically de’fined process, isa highly controlled type of cell death that plays a critical role in embryonic development, deletion of aLAoreaclive T-cells and adult tissue homoeostasis. There is increasing evidence thaI derangement of the epoptotic program is the underlying cause of a series of diseases including liver diseases. The deadly program can be initiated by ligand binding to membrane bound receptors such as CD95, which is the most prominent cell death inducing member of the Tumor necrosis factor (TN’F) receptor superfamily. The core of the subsequently activated intracellular machinery is formed by a set of proleases, namely caspasss. Once activated, they orchestrate the complete destruction of the cellular skeleton leadiing to the typical apoptotlc morphology. (Schuchmann & Ga’lIe, 2001). Tumor necrosis factor (TNFl. fibroblast-associated cell surface (Fas) Ugand, and TNF-related apoptosis-inducing ligand (TRAIL), all members of the TNF superfamily, are arguably the most potent inducers of cell death. These cytokines induce cell death through sequential recruitment by the death receptors TNFR1- associated death domain protein (TRAOD), Fa.s-associateddeath domain protein (FADD), FADDlike interleukin-1beta-converting enzyme (FLlCE), and downstream |