By John F. R. Kerr (auth.), Dr. Sharad Kumar (eds.)
The prior few years have visible swift growth in apoptosis learn. This quantity bargains with a number of the fresh advances made in uncovering the molecular and mobile foundation of apoptosis, with specific emphasis to the position of apoptosis in basic organic approaches and the mechanisms concerned.
The articles released during this quantity are written by way of prime 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
1995}. Gene targeting and transgene technologies have been used in order to unravel the in vivo role of the TNF/TNF-Rs system and to establish genetically defined models of human diseases. TNF_,_ mi ce show an almost normal phenotype histologically, but have reduced sensitivity to lipopolysoccharide (LPS)-mediated toxicity and increased sensitivity to intracellular pathogens like Listeria, due to severely impaired macrophage function (Pasparakis et al. 1996}. Moreover, they lack typical germinal center formation and, although capable of undergoing IgG and IgE class switching, show quantitative differences in the Ig composition of secondary antibody responses.
Stimuli (Brockhaus et al. 1990; Thoma et al. 1990). TNF-R1 is responsible for most of the biologica! properties of TNF, including programmed cell death, antiviral activity, and activation of the transcription factor NF-KB in a wide varietyof cell types (Engelmann et al. 1990; Espevik et al. 1990; Tartaglia et al. 1991, 1993a; Wong et al. 1992). It also plays an essential role in the host defense against microorganisms and bacterial pathogens (Pfeffer et al. 1993; Rothe et al. 1993). The contribution of TNF-R2 to cellular responses induced by sTNF appears tobe of a supportive or modulating nature, with two distinct functional properties.
1993; Hiramatsu et al. 1994; Galle et al. 1995), whereas expression of CD95L is more tightly regulated. Originally, expression of the ligand seemed tobe restricted to T cells (Suda et al. 1993), but turned out to be expressed in some important nonlymphoid areas as discussed below. Identification of CD95 and CD95L helped to explain the phenotype of two mutant mice: lpr (for lymphoproliferation) (Watanabe-Fukunaga et al. 1992a) and gld (for generalized lymphoproliferative disease) (Takahashi et al.
Apoptosis: Biology and Mechanisms by John F. R. Kerr (auth.), Dr. Sharad Kumar (eds.)