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641
Oxygen stress: a regulator of apoptosis in yeast
- J. Cell
, 1999
"... Abstract. Oxygen radicals are important components of metazoan apoptosis. We have found that apoptosis can be induced in the yeast Saccharomyces cerevisiae by depletion of glutathione or by low external doses of H 2O 2. Cycloheximide prevents apoptotic death revealing active participation of the cel ..."
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Cited by 126 (9 self)
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Abstract. Oxygen radicals are important components of metazoan apoptosis. We have found that apoptosis can be induced in the yeast Saccharomyces cerevisiae by depletion of glutathione or by low external doses of H 2O 2. Cycloheximide prevents apoptotic death revealing active participation of the cell. Yeast can also be triggered into apoptosis by a mutation in CDC48 or by expression of mammalian bax. In both cases, we show oxygen radicals to accumulate in the cell, whereas radical depletion or hypoxia prevents apoptosis. These results suggest that the generation of oxygen radicals is a key event in the ancestral apoptotic pathway and offer an explanation for the mechanism of bax-induced apoptosis in the absence of any established apoptotic gene in yeast.
Apoptosis in resolution of inflammation
- J. Leukoc. Biol
, 1997
"... Abstract: The last few years have seen the accumulation of compelling evidence that apoptosis (programmed cell death) plays a major role in promoting resolution of the acute inflammatory response. Neutropulls are constitutively programmed to undergo apoptosis, which limits their pro-inflammatory pot ..."
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Cited by 102 (2 self)
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Abstract: The last few years have seen the accumulation of compelling evidence that apoptosis (programmed cell death) plays a major role in promoting resolution of the acute inflammatory response. Neutropulls are constitutively programmed to undergo apoptosis, which limits their pro-inflammatory potential and leads to rapid, specific, and non-phlogistic recognition by macrophages and semi-professional phagocytes. Similar mechanisms have been implicated in clearance ofeosinophils, lymphocytes, and monocytes and apoptosis also plays a role in remodeling the inflamed site by deletion of myofibroblasts. A growing understanding ofthe mechanisms regulating leukocyte apoptosis and ofthe molecules mediating safe phagocytic clearance of dying cells may yield new insights into the pathogenesis and therapy of inflammatory diseases.
A yeast mutant showing diagnostic markers of early and late apoptosis
- J. Cell
, 1997
"... Abstract. A Saccharomyces cerevisiae mutant in cell division cycle gene CDC48 shows typical markers of apoptosis: membrane staining with annexin V, indicating an exposure of phosphatidylserine at the outer layer of the cytoplasmic membrane; intense staining, using the terminal deoxynucleotidyl trans ..."
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Cited by 90 (10 self)
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Abstract. A Saccharomyces cerevisiae mutant in cell division cycle gene CDC48 shows typical markers of apoptosis: membrane staining with annexin V, indicating an exposure of phosphatidylserine at the outer layer of the cytoplasmic membrane; intense staining, using the terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling method, indicating DNA fragmentation; and chromatin condensation and fragmentation. The coordinate occurrence of these events at different locations in the cell, which have no obvious connection except their relation to apoptosis, implies the presence of the molecular machinery performing the basic steps of apoptosis already in yeast. Saccharomyces cerevisiae may prove a suitable model to trace the roots of apoptosis. Apoptosis is a form of programmed cell death with an important role in development and homeostasis of metazoan organisms. Apoptosis allows the rapid removal of unwanted or damaged cells that could otherwise inflame the surrounding cells with their cytoplasmic contents. In contrast, during necrosis, a form of cell death that results from overwhelming cellular injury, cells lyse and release cytoplasmic material. The apoptotic program is switched on in irreparably damaged or potentially dangerous cells such as self-reactive lymphocytes or cells that have been infected by viruses. Furthermore, it is involved in tumor suppression and in a wide range of diseases such as AIDS, neurodegenerative processes, and ischemic stroke
The Reliability Theory of Aging and Longevity
- JOURNAL OF THEORETICAL BIOLOGY
, 2001
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Proteases for cell suicide: functions and regulation of caspases
- Microbiol. Mol. Biol. Rev
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Apoptosis reduces both the in vitro replication and the in vivo infectivity of a baculovirus
- J
, 1993
"... and the in vivo infectivity of a baculovirus. Apoptosis reduces both the in vitro replication ..."
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Cited by 50 (11 self)
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and the in vivo infectivity of a baculovirus. Apoptosis reduces both the in vitro replication
Inhibition of anchorage-dependent cell spreading triggers apoptosis in cultured human endothelial cells
- J. Cell
, 1994
"... Abstract. When cultivated on substrates that prevent cell adhesion (the polymer polyhydroxyethylmethacrylate, bovine serum albumin, and Teflon), human endothelial cells (EC) rapidly lost viability with a halflife of,x,10 h. Dying EC showed the morphological and biochemical characteristics of apoptos ..."
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Cited by 40 (0 self)
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Abstract. When cultivated on substrates that prevent cell adhesion (the polymer polyhydroxyethylmethacrylate, bovine serum albumin, and Teflon), human endothelial cells (EC) rapidly lost viability with a halflife of,x,10 h. Dying EC showed the morphological and biochemical characteristics of apoptosis. The apoptotic process of suspended EC was delayed by the protein synthesis inhibitor cycloheximide. To obtain information as to the mechanism involved in the apoptosis of suspended EC, we investigated whether adhesion to matrix proteins or integrin occupancy in EC retaining a round shape may affect EC suicide. EC bound to low coating concentration of either fibronectin or vitronectin, retaining a round shape and failing to organize actin microfilaments, underwent to rapid
Temporal analysis of events associated with programmed cell death (apoptosis) of sympathetic neurons deprived of nerve growth factor
- J. Cell
, 1993
"... Abstract. The time course of molecular events that accompany degeneration and death after nerve growth factor (NGF) deprivation and neuroprotection by NGF and other agents was examined in cultures of NGFdependent neonatal rat sympathetic neurons and compared to death by apoptosis. Within 12 h after ..."
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Cited by 37 (5 self)
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Abstract. The time course of molecular events that accompany degeneration and death after nerve growth factor (NGF) deprivation and neuroprotection by NGF and other agents was examined in cultures of NGFdependent neonatal rat sympathetic neurons and compared to death by apoptosis. Within 12 h after onset of NGF deprivation, glucose uptake, protein synthesis, and RNA synthesis fell precipitously followed by a moderate decrease of mitochondrial function. The molecular mechanisms underlying the NGF deprivation-induced decrease of protein synthesis and neuronal death were compared and found to be different, demonstrating that this decrease of protein synthesis is insufficient to cause death subsequently. After these early changes and during the onset of neuronal atrophy,
A Role for Caspases in Lens Fiber Differentiation
"... Abstract. There is increasing evidence that programmed cell death (PCD) depends on a novel family of intracellular cysteine proteases, called caspases, that includes the Ced-3 protease in the nematode Caenorhabditis elegans and the interleukin-1�–converting enzyme (ICE)-like proteases in mammals. So ..."
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Cited by 32 (0 self)
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Abstract. There is increasing evidence that programmed cell death (PCD) depends on a novel family of intracellular cysteine proteases, called caspases, that includes the Ced-3 protease in the nematode Caenorhabditis elegans and the interleukin-1�–converting enzyme (ICE)-like proteases in mammals. Some developing cells, including lens epithelial cells, erythroblasts, and keratinocytes, lose their nucleus and other organelles when they terminally differentiate, but it is not known whether the enzymatic machinery of PCD is involved in any of these normal differentiation events. We show here that at least one CPP32 (caspase-3)-like member of the caspase family becomes activated when rodent lens epithelial cells terminally differentiate into anucleate lens fibers in vivo, and that a peptide inhibitor
Growth arrest and autophagy are required for salivary gland cell degradation in Drosophila. Cell 131
, 2007
"... Autophagy is a catabolic process that is nega-tively regulated by growth and has been impli-cated in cell death. We find that autophagy is induced following growth arrest and precedes developmental autophagic cell death of Drosophila salivary glands. Maintaining growth by expression of either activa ..."
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Cited by 32 (0 self)
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Autophagy is a catabolic process that is nega-tively regulated by growth and has been impli-cated in cell death. We find that autophagy is induced following growth arrest and precedes developmental autophagic cell death of Drosophila salivary glands. Maintaining growth by expression of either activatedRas or positive regulators of the class I phosphoinositide 3-kinase (PI3K) pathway inhibits autophagy and blocks salivary gland cell degradation.Develop-mental degradation of salivary glands is also inhibited in autophagy gene (atg) mutants. Cas-pases are active in PI3K-expressing and atg mutant salivary glands, and combined inhibition of both autophagy and caspases increases suppression of gland degradation. Further, induction of autophagy is sufficient to induce premature cell death in a caspase-independent manner. Our results provide in vivo evidence that growth arrest, autophagy, and atg genes are required for physiological autophagic cell death and that multiple degradation pathways cooperate in the efficient clearance of cells during development.