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Induction of apoptosis by cancer chemotherapy.

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TLDR
The two prototypic death pathways are described, current understanding of the role of the two pathways in chemotherapy-induced apoptosis is summarized, and the implications of these studies for mechanisms of resistance to chemotherapeutic agents are discussed.
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This article is published in Experimental Cell Research.The article was published on 2000-04-10. It has received 1226 citations till now. The article focuses on the topics: Fas ligand & Apoptosis.

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Mammalian caspases: structure ,a ctivation ,s ubstrates, and functions during apoptosis

TL;DR: Caspases, a family of cysteine-dependent aspartate-directed proteases, are prominent among the death proteases as discussed by the authors, and they play critical roles in initiation and execution of this process.
Journal ArticleDOI

Modulation of oxidative stress as an anticancer strategy.

TL;DR: The controversial role of ROS in tumour development and in responses to anticancer therapies is addressed, and the idea that targeting the antioxidant capacity of tumour cells can have a positive therapeutic impact is elaborate.
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The cellular and molecular basis of hyperthermia.

TL;DR: The direct cytotoxic effect of heat, heat-induced alterations of the tumor microenvironment, synergism of heat in conjunction with radiation and drugs, as well as, the presumed cellular effects of hyperthermia including the expression of heat-shock proteins (HSP), induction and regulation of apoptosis, signal transduction, and modulation of drug resistance byhyperthermia are discussed.
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MicroRNA: Biogenesis, Function and Role in Cancer.

TL;DR: The P-body model outlines microRNA sorting and shuttling between specialized P- body compartments that house enzymes required for slicer –dependent and –independent silencing, addressing the reversibility of these silencing mechanisms.
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Oxidative stress: the mitochondria-dependent and mitochondria-independent pathways of apoptosis

TL;DR: This review highlights the basic mechanisms of ROS production and their sites of formation; detail mechanism of both mitochondria-dependent and mitochondrial-independent pathways of apoptosis as well as their regulation by ROS and describes the involvement of oxidative stress under various environmental toxin- and drug-induced organ pathophysiology and diabetes-mediated apoptosis.
References
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Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade

TL;DR: Mutation of the active site of caspase-9 attenuated the activation of cazase-3 and cellular apoptotic response in vivo, indicating that casp enzyme-9 is the most upstream member of the apoptotic protease cascade that is triggered by cytochrome c and dATP.
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Molecular characterization of mitochondrial apoptosis-inducing factor

TL;DR: The identification and cloning of an apoptosis-inducing factor, AIF, which is sufficient to induce apoptosis of isolated nuclei is reported, indicating that AIF is a mitochondrial effector of apoptotic cell death.
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BCL-2 family members and the mitochondria in apoptosis

TL;DR: As the BCL-2 family members reside upstream of irreversible cellular damage and focus much of their efforts at the level of mitochondria, they play a pivotal role in deciding whether a cell will live or die, and it is argued that the amphipathic a-helical BH3 domain serves as a critical death domain in the pro-apoptotic members.
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Regulation of Cell Death Protease Caspase-9 by Phosphorylation

TL;DR: In this paper, the kinase Akt and p21-Ras, an Akt activator, induced phosphorylation of pro-caspase-9 (pro-Casp9) in cells.
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A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD

TL;DR: A caspase-activated deoxyribonuclease (CAD) and its inhibitor (ICAD) have now been identified in the cytoplasmic fraction of mouse lymphoma cells and seems to function as a chaperone for CAD during its synthesis, remaining complexed with CAD to inhibit its DNase activity.
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