Apoptosis: Biology and Mechanisms - download pdf or read online

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

ISBN-10: 3540691847

ISBN-13: 9783540691846

ISBN-10: 366221623X

ISBN-13: 9783662216231

The previous few years have noticeable speedy growth in apoptosis examine. This quantity offers with a few of the contemporary advances made in uncovering the molecular and mobile foundation of apoptosis, with specific emphasis to the function of apoptosis in basic organic procedures and the mechanisms concerned.
The articles released during this quantity are written via best specialists within the box and may be an important source for researchers in biomedicine.

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Extra resources for Apoptosis: Biology and Mechanisms

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Cient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair. J. B, Ferenz CR, Franklin S, Ghayur T, Hackett MC, Hamill LD, Herzog L, Hugunin M, Houy W, Mankovich JA, McGuiness L, Orlewicz E, Paskind M, Pratt CA, Reis P, Summani A, Terranova M, Welch JP, Xiong L, Mtiller A, Tracey DE, Kamen R, Wong WW (1994) Crystal structure of the cysteine protease interleukin-1-~­ converting enzyme: a (p20/p10) 2 homodimer. Cell 78:343-352 Wang ZQ, Auer B, Stingi L, Berghammer H, Haidacher D, Schweiger M, Wagner EF (1995) Mice lacking ADPRT and poly(ADP-ribosyl)ation develop normally but are susceptible to skin disease.

Peter et al. distinct kinetics of ligand association and dissociation of the two receptors (Tartaglia et al. 1993b). However, the prime physiological activator ofTNF-R2 seems tobe mTNF, since TNF-R2 can be strongly stimulated by mTNF rather than by sTNF. As mTNF also signals via TNF-R1, the resulting cooperativity of both receptors leads to cellular responses much stronger than those achievable with sTNF alone. Moreover, it was shown that upon appropriate activation of TNF-R2, a phenotypic switch of the cellular response pattern to TNF could be observed, such that, as an example, cells fully resistant to the cytotoxic action of sTNF become highly susceptible and are killed upon contact with mTNF (Grell et al.

1996). In vitro, granzyme B can cleave a number of caspase precursor polypeptides, leading to their activation, and it is also capable of cleaving some of the same substrates as certain caspases. These observations have led to speculation that granzyme B in CTL causes target cell death by activating the caspases or by replacing them. 8 Apoptosis in Disease Although apoptosis ultimately serves to benefit the organism, malfunction in the regulation of this process can result in various pathological states.

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


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