By John F. R. Kerr (auth.), Dr. Sharad Kumar (eds.)

The earlier few years have noticeable swift growth in apoptosis study. This quantity offers with a number of the contemporary advances made in uncovering the molecular and mobile foundation of apoptosis, with specific emphasis to the function of apoptosis in common organic strategies and the mechanisms concerned.
The articles released during this quantity are written by means of top specialists within the box and may be an important source for researchers in biomedicine.

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Together with the receptor, these proteins formed the death-inducing signaling complex (DISC). Using a specific rabbit antiserum CAPI and 2 could be identified as two different serine phosphorylated species ofFADD and demonstrated that FADD bound to CD95 in a stimulation-dependent fashion in vivo. Overexpression of the N-terminal half of FADD induced cell death (Chinnaiyan et al. 1995). This part of FADD 34 M. E. Peter et al. was therefore termed the death effector domain (DED). Overexpression ofthe C-terminal DD-containing part (FADD-DN), however, protected cells from CD95-mediated apoptosis and functioned as a dominant negative.

1992; WatanabeFukunaga et al. 1992b). By comparing CD95 with TNF-R1, a domain was identified in the intracellular tail of both receptors that was essential for transduction of a death signal into cells (Itoh and Nagata 1993; Tartaglia et al. 1993a}. It was called the death domain (DD). Surprisingly, it took 4 years to identify other receptors that carry a DD in their intracellular part. DR3 (TRAMP/wsl-1/AP0-3/LARD/AIR) is both structurally and functionally similar to TNF-Rl whereas DR4/TRAIL-Rl is functionally similar to CD95 as its main function seems tobe to induce apoptosis (Pan et al.

1995; Freiberg et al. 1997), the overall in vitro and in vivo data suggest that CD95 is a receptor which mainly mediates apoptosis. The physiological role of the CD95/CD95L system seems to be strongly connected to the immune system and to the liver (Adachi et al. 1995). It could be shown that after T cell receptor engagement on previously activated or transformed T cells (Alderson et al. 1995; Brunner et al. 1995; Dhein et al. The Death Receptors 29 1995; Ju et al. 1995), CD95L expression is upregulated, and cells then undergo apoptosis due to CD95/CD95L interactions.

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