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ERK and cell death: Mechanisms of ERK‐induced cell death – apoptosis, autophagy and senescence

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TLDR
The Ras/Raf/extracellular signal‐regulated kinase (ERK) signaling pathway plays a crucial role in almost all cell functions and therefore requires exquisite control of its spatiotemporal activity.
Abstract
The Ras/Raf/extracellular signal-regulated kinase (ERK) signaling pathway plays a crucial role in almost all cell functions and therefore requires exquisite control of its spatiotemporal activity. Depending on the cell type and stimulus, ERK activity will mediate different antiproliferative events, such as apoptosis, autophagy and senescence in vitro and in vivo. ERK activity can promote either intrinsic or extrinsic apoptotic pathways by induction of mitochondrial cytochrome c release or caspase-8 activation, permanent cell cycle arrest or autophagic vacuolization. These unusual effects require sustained ERK activity in specific subcellular compartments and could depend on the presence of reactive oxygen species. We will summarize the mechanisms involved in Ras/Raf/ERK antiproliferative functions.

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Signal Transduction in Cancer

TL;DR: An examination of the PI3K-Akt and Ras-ERK pathways illustrates how such alterations dysregulate signaling in cancer and produce many of the characteristic features of tumor cells.
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Anti-apoptosis and cell survival: A review

TL;DR: This work discusses the different strategies that are used to prevent cell death and illustrates that although anti-apoptosis and cellular survival serve to counteract PCD, they are nevertheless mechanistically distinct from the processes that regulate cell death.
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Thioredoxins, glutaredoxins, and peroxiredoxins--molecular mechanisms and health significance: from cofactors to antioxidants to redox signaling.

TL;DR: This review summarizes the almost 50 years of research on these proteins, focusing primarily on data from vertebrates and mammals, that is, their potential impact and functions in different cell types, tissues, and various pathological conditions.
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Understanding MAPK Signaling Pathways in Apoptosis.

TL;DR: This review presents the main pro- and anti-apoptotic mechanisms regulated by MAPKs, as well as the crosstalk observed between some MAPKS, and describes the basic signaling properties ofMAPKs (ultrasensitivity, hysteresis, digital response), and the presence of different positive feedback loops in apoptosis.
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Mitochondrial regulation of cell cycle and proliferation.

TL;DR: The traffic of the different canonical signaling pathways to mitochondria and the contributions of organelles to redox regulation of kinases are highlighted and the dynamics of the mitochondrial population in cell cycle and apoptosis are analyzed.
References
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Journal ArticleDOI

Self-eating and self-killing: crosstalk between autophagy and apoptosis

TL;DR: The functional relationship between apoptosis and autophagy is complex in the sense that, under certain circumstances,autophagy constitutes a stress adaptation that avoids cell death (and suppresses apoptosis), whereas in other cellular settings, it constitutes an alternative cell-death pathway.
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Apoptosis: controlled demolition at the cellular level

TL;DR: This work has shown that during the demolition phase of apoptosis, members of the caspase family of cysteine proteases target several hundred proteins for restricted proteolysis in a controlled manner that minimizes damage and disruption to neighbouring cells and avoids the release of immunostimulatory molecules.
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BRAFE600-associated senescence-like cell cycle arrest of human naevi

TL;DR: It is shown that sustained BRAFV600E expression in human melanocytes induces cell cycle arrest, which is accompanied by the induction of both p16INK4a and senescence-associated acidic β-galactosidase (SA-β-Gal) activity, a commonly usedsenescence marker.
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cPLA2 is phosphorylated and activated by MAP kinase.

TL;DR: Treatment of cells with agents that stimulate the release of arachidonic acid causes increased serine phosphorylation and activation of cytosolic phospholipase A2 (cPLA2).
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Reactive Oxygen Species Promote TNFα-Induced Death and Sustained JNK Activation by Inhibiting MAP Kinase Phosphatases

TL;DR: It is shown that TNFalpha-induced ROS, whose accumulation is suppressed by mitochondrial superoxide dismutase, cause oxidation and inhibition of JNK-inactivating phosphatases by converting their catalytic cysteine to sulfenic acid, which results in sustained JNK activation, which is required for cytochrome c release and caspase 3 cleavage.
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