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PMID:15680329

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Citation

Lum, JJ, Bauer, DE, Kong, M, Harris, MH, Li, C, Lindsten, T and Thompson, CB (2005) Growth factor regulation of autophagy and cell survival in the absence of apoptosis. Cell 120:237-48

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.

Links

PubMed Online version:10.1016/j.cell.2004.11.046

Keywords

Animals; Apoptosis/physiology; Autophagy/physiology; Bone Marrow Cells/metabolism; Bone Marrow Cells/ultrastructure; DNA Fragmentation/physiology; Glycolysis/physiology; Growth Substances/deficiency; Interleukin-3/metabolism; Lysosomes/metabolism; Lysosomes/ultrastructure; Mice; Mice, Knockout; Microscopy, Electron, Transmission; Mitochondria/metabolism; Mitochondria/ultrastructure; Proto-Oncogene Proteins c-bcl-2/metabolism; bcl-2-Associated X Protein

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


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References

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