By Stefan Grimm
Apoptosis is an important method in embryonic improvement and tissue homeostasis, relatively within the prevention of affliction. Written from a genetic perspective, Genetics of Apoptosis first describes the molecular and phone biology of apoptosis, then examines the method in additional aspect in numerous version structures. This quantity brings jointly contributions from the world over popular authors, and should be a priceless connection with all researchers learning apoptosis.
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Extra resources for Genetics of Apoptosis
2000). , 2000). RelA-/- fibroblasts, unlike their wild-type (RelA+/+) counterparts, exhibit a profound sensitivity to TNF-α-induced apoptosis (Beg and Baltimore, 1996). , 2001b). These observations demonstrate an important role of NF-κB in protecting cells from death receptor-induced apoptosis. Engagement of TNFR1 by TNF leads to the recruitment of the adapter protein TRADD to the clustered DDs of the trimerized receptors. TRADD, in turn, serves as a platform for the docking of multiple signaling molecules to the activated receptor complex.
It will be important to determine whether interruption of a distal step of the death-signaling pathway shared by CD95L and granzyme B (such as loss of BAX/BAK) reduces CTL-induced death of type II target cells that require cross-talk between the extrinsic and intrinsic pathways to undergo apoptosis. Such genetic impediments to CTL-induced death may be an important mechanism by which tumor cells evade immune surveillance. Establishment of zones of immune privilege Immune-privileged sites such as the eye, brain, and the testes may evade damage by constitutively expressing CD95L to counterattack and eliminate CD95-expressing infiltrating lymphocytes (Green and Ferguson, 2001).
The following mechanistic links between the intrinsic and extrinsic pathways may account for the synergistic cytotoxicity of chemotherapeutic agents/irradiation and death ligands: (1) DNA damage promotes expression of the death receptors (CD95 and DR5/TRAIL-R2). (2) Cellular damage inflicted by chemotherapeutic agents can promote expression of BAK. (3) p53 may inhibit the transcriptional activity of NF-κB. Although death receptors play contributory, yet dispensable, roles in the response to conventional chemotherapy or irradiation, death receptor-ligand interactions may be instrumental for the action of cancer immunotherapy or specific anticancer agents.