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Lum, J. J., Bauer, D. E., Kong, M., Harris, M. H., Li, C., & Lindsten, T., et al. (2005). Growth Factor Regulation of Autophagy and Cell Survival in the Absence of Apoptosis. Cell, 120(2), 237–248. 
Added by: Dr. Enrique Feoli (05/01/2021, 20:24)   Last edited by: Dr. Enrique Feoli (05/01/2021, 20:25)
Resource type: Journal Article
DOI: 10.1016/j.cell.2004.11.046
ID no. (ISBN etc.): 0092-8674
BibTeX citation key: Lum2005
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Categories: BioAcyl Corp
Subcategories: Bioenergetics
Creators: Bauer, Harris, Kong, Li, Lindsten, Lum, Thompson
Collection: Cell
Views: 2/892
Abstract
In animals, cells are dependent on extracellular signals to prevent apoptosis. However, using growth factor-dependent cells from Bax/Bak-deficient mice, we demonstrate that apoptosis is not essential to limit cell autonomous survival. Following growth factor withdrawal, Bax−/−Bak−/− cells activate autophagy, undergo progressive atrophy, and ultimately succumb to death. These effects result from loss of the ability to take up sufficient nutrients to maintain cellular bioenergetics. Despite abundant extracellular nutrients, growth factor-deprived cells maintain ATP production from catabolism of intracellular substrates through autophagy. Autophagy is essential for maintaining cell survival following growth factor withdrawal and can sustain viability for several weeks. During this time, cells respond to growth factor readdition by rapid restoration of the ability to take up and metabolize glucose and by subsequent recovery of their original size and proliferative potential. Thus, growth factor signal transduction is required to direct the utilization of sufficient exogenous nutrients to maintain cell viability.
  
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