By Stefan Grimm
Apoptosis is a vital technique in embryonic improvement and tissue homeostasis, relatively within the prevention of ailment. Written from a genetic perspective, Genetics of Apoptosis first describes the molecular and telephone biology of apoptosis, then examines the method in additional element in different version platforms. This quantity brings jointly contributions from across the world well known authors, and should be a important connection with all researchers learning apoptosis.
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Additional info for Genetics of Apoptosis
While FasL is unable to activate NF-κB, TNF-α induces activation of the transcription factors, NF-κB and JNK/AP1, via recruitment of receptorinteracting protein (RIP) and TNFR-associated factor-2 (TRAF-2) to the receptor complex. , 1998; Scheidereit, 1998). , 1998). , 1997). , 1998). Therefore, RIP is essential for TNF-induced activation of NF-κB, while TRAF2 is required for signaling the activation of JNK. In addition to inducing expression of diverse proinflammatory and immunomodulatory genes, NF-κB promotes the expression of genes that protect cells from TNF-induced apoptosis (discussed below).
2001). These findings indicate that the death receptor and DNA damage/stress-induced signaling pathways operate largely independently until they converge at the level of mitochondrial disruption (Figure 3). 28 GENETICS OF APOPTOSIS Figure 3. Cross-talk between the death receptor (extrinsic) and stress-induced (intrinsic/ mitochondrial) death signaling pathways. Cellular stress or DNA damage results in stabilization of p53. p53 can promote mitochondrial activation of caspase-9/Apaf-1 by inducing the expression of specific target genes, such as Noxa, PUMA, or Bax.
The molecular regulation of cell survival is a fundamental determinant of lymphocyte maturation, receptor repertoire selection, homeostasis, and the cellular response to stressful stimuli, such as DNA damage (Krammer, 2000). Increased apoptosis is involved in the pathogenesis of diverse immune disorders. Conversely, genetic aberrations that render cells incapable of executing their suicide program result in autoimmune disorders and tumorigenesis. The physiologic role played by death receptors in the immune response is summarized below.