Download Apoptosis: Biology and Mechanisms by John F. R. Kerr (auth.), Dr. Sharad Kumar (eds.) PDF

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

ISBN-10: 366221623X

ISBN-13: 9783662216231

The earlier few years have obvious quick growth in apoptosis study. This quantity bargains with a few of the fresh advances made in uncovering the molecular and mobile foundation of apoptosis, with specific emphasis to the position of apoptosis in general organic tactics and the mechanisms concerned.
The articles released during this quantity are written via major specialists within the box and will be a necessary source for researchers in biomedicine.

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Extra info for Apoptosis: Biology and Mechanisms

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G. Liu et al. 1996; Van Antwerp et al. 1996; Wang et al. 1996a; Wu et al. 1996). Conversely, expression of the NF-KB inhibitor I-KBa breaks this resistance. Furthermore, embryonic fibroblasts from c-Rel_ 1_ mice readily die upon TNF treatment in the absence of Chx while the c-Rel+t+ cells are completely resistant (Beg and Baltimore 1996; Van Antwerp et al. 1996). As described, A20 is a good candidate for such an anti-apoptosis gene since it is driven by NF-KB and inhibits TNF-induced apoptosis (Krikos et al.

However, overexpression of a DED containing molecule such as caspase-8 or FADD could just block any other DED protein binding to the receptor and thereby block the signaling pathway. Consistent with this assumption, we and others have not been able to detect a direct interaction of FADD with TNF-R1 (unpubl. -B. Shu and D. Goeddel, pers. ). g. a FADD-like molecule) or FADD couples indirectly to this receptor (Fig. 2). Therefore, the question whether caspase-8 would be activated by TNF-R1 was believed to provide an answer to this question.

1993). The gld defect arises from a point mutation within the gene encoding CD95L, changing an amino acid critica! for CD95 binding. In humans a similar disease was reported (Fisher et al. 1995; Rieux-Laucat et al. 1995), with a dysfunction of the CD95/CD95L system. Children with this "autoimmune lymphoproliferative syndrome" (ALPS) have massive, nonmalignant lymphadenopathy, an altered and enlarged T cell population and a massive autoimmune disorder. Although there are a few reports showing that triggering of CD95 results in secretion of IL-8 (Abreu-Martin et al.

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