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Nat Cell Biol. 2014 Aug;16(8):728-36. doi: 10.1038/ncb3005.

Organelle-specific initiation of cell death.

Author information

1
1] Equipe 11 labellisée par la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France [2] Université Paris Descartes/Paris V, Sorbonne Paris Cité, Paris, France [3] Gustave Roussy Comprehensive Cancer Center, Villejuif, France.
2
1] Equipe 11 labellisée par la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France [2] Gustave Roussy Comprehensive Cancer Center, Villejuif, France [3] INSERM, U1138, Villejuif, France.
3
1] Equipe 11 labellisée par la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France [2] Université Paris Descartes/Paris V, Sorbonne Paris Cité, Paris, France [3] INSERM, U1138, Villejuif, France [4] Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, Paris, France [5] Metabolomics and Cell Biology Platforms, Gustave Roussy Comprehensive Cancer Center, Villejuif, France.

Abstract

In a majority of pathophysiological settings, cell death is not accidental - it is controlled by a complex molecular apparatus. Such a system operates like a computer: it receives several inputs that inform on the current state of the cell and the extracellular microenvironment, integrates them and generates an output. Thus, depending on a network of signals generated at specific subcellular sites, cells can respond to stress by attemptinwg to recover homeostasis or by activating molecular cascades that lead to cell death by apoptosis or necrosis. Here, we discuss the mechanisms whereby cellular compartments - including the nucleus, mitochondria, plasma membrane, endoplasmic reticulum, Golgi apparatus, lysosomes, cytoskeleton and cytosol - sense homeostatic perturbations and translate them into a cell-death-initiating signal.

PMID:
25082195
DOI:
10.1038/ncb3005
[Indexed for MEDLINE]

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