Download Apoptosis and Cancer Therapy: From Cutting-edge Science to by Klaus-Michael Debatin, Simone Fulda, Editors PDF

By Klaus-Michael Debatin, Simone Fulda, Editors

Right here, a global and hugely wonderful crew of authors leads readers from the foundations of programmed cellphone loss of life to the function of apoptosis in melanoma improvement and rising therapy concepts. Divided into special elements, the 1st specializes in apoptosis signaling, protecting intensive such issues as mitochondria, effector platforms, the Bcl-2 relatives, IAPs, survival pathways, tumor suppressor genes, modulators, lysosomes and phagocytosis. the second one part is going directly to learn apoptosis in melanoma and melanoma treatment, with a close examine version platforms, molecular analysis, mobile rigidity, DNA harm and service, molecular ambitions and healing elements. With its powerful specialize in contemporary advancements in melanoma remedy, this e-book is aimed toward oncologists, molecular and cellphone biologists, biochemists, and people operating within the pharmaceutical and biotechnological industries.

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Extra info for Apoptosis and Cancer Therapy: From Cutting-edge Science to Novel Therapeutic Concepts

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Another mechanism by which tumors interfere with DR-mediated apoptosis may be the expression of soluble receptors that act as decoys for death ligands. To date, two soluble receptors – soluble CD95 (sCD95) and decoy receptor 3 (DcR3) – competitively inhibit CD95 signaling. sCD95 is elevated in several autoimmune disorders and in the sera of certain cancer patients. High sCD95 serum levels were associated with a poor prognosis in melanoma patients [79, 80]. DcR3 interacts with CD95L and thereby inhibits CD95L-induced apoptosis.

Cytochrome c is an important component of the mitochondrial respiratory chain and the best-characterized proapoptotic protein of mitochondrial origin [9]. The release of cytochrome c into the cytosol results in ATP-dependent oligomerization of the adapter apoptosis-inducing factor 1 (Apaf-1) and recruitment of procaspase-9. Consequently, a supramolecular complex called an “apoptosome” is formed. Caspase-9 bound to the apoptosome activates downstream effector caspases such as caspase-3 [15]. Another protein released from the mitochondria upon induction of apoptosis is Smac/DIABLO.

Upon translocation into the nucleus activated NF-AT initiates gene transcription and is thus regarded as one of the key participants in CD95L regulation [64]. ZAP-70 is also involved in activation of protein kinase C (PKC). The u isoform of PKC has been shown to be essential for activation-induced CD95L expression [64] and for TCR-induced NF-kB activation [65]. Activated NF-kB was shown to be required for high expression levels of CD95L in T cells [66–69]. Activation of T cells via TCR also leads to a Ras-activated cascade of kinase activity including Raf, Mek, Erk and p38 mitogen-activated tyrosine kinase (MAPK).

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