Eisenberg-Lerner, A; Bialik, S; Simon, H-U; Kimchi, A (2009). Life and death partners: apoptosis, autophagy and the cross-talk between them. Cell death and differentiation, 16(7), pp. 966-75. Basingstoke: Nature Publishing Group 10.1038/cdd.2009.33
Full text not available from this repository.It is not surprising that the demise of a cell is a complex well-controlled process. Apoptosis, the first genetically programmed death process identified, has been extensively studied and its contribution to the pathogenesis of disease well documented. Yet, apoptosis does not function alone to determine a cell's fate. More recently, autophagy, a process in which de novo-formed membrane-enclosed vesicles engulf and consume cellular components, has been shown to engage in a complex interplay with apoptosis. In some cellular settings, it can serve as a cell survival pathway, suppressing apoptosis, and in others, it can lead to death itself, either in collaboration with apoptosis or as a back-up mechanism when the former is defective. The molecular regulators of both pathways are inter-connected; numerous death stimuli are capable of activating either pathway, and both pathways share several genes that are critical for their respective execution. The cross-talk between apoptosis and autophagy is therefore quite complex, and sometimes contradictory, but surely critical to the overall fate of the cell. Furthermore, the cross-talk is a key factor in the outcome of death-related pathologies such as cancer, its development and treatment.
Item Type: |
Journal Article (Further Contribution) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Pharmacology |
UniBE Contributor: |
Simon, Hans-Uwe |
ISSN: |
1350-9047 |
Publisher: |
Nature Publishing Group |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 15:10 |
Last Modified: |
05 Dec 2022 14:21 |
Publisher DOI: |
10.1038/cdd.2009.33 |
PubMed ID: |
19325568 |
Web of Science ID: |
000267496200006 |
URI: |
https://boris.unibe.ch/id/eprint/30713 (FactScience: 194991) |
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