Journal
MOLECULAR CELL
Volume 40, Issue 2, Pages 280-293Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2010.09.023
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Funding
- Ligue Nationale contre le Cancer
- Agence Nationale pour la Recherche (ANR)
- European Commission
- Fondation pour la Recherche Medicale (FRM)
- Institut National du Cancer (INCa)
- Canceropole Ile-de-France
- AXA Chair for Longevity Research
- EMBO
- National Institutes of Health (NIH)
- National Cancer Institute (NCI)/National Institute of Allergy and Infectious Diseases (NIAID)
- Howard Hughes Medical Institute (HHMI)
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Autophagy is a tightly regulated pathway involving the lysosomal degradation of cytoplasmic organelles or cytosolic components. This pathway can be stimulated by multiple forms of cellular stress, including nutrient or growth factor deprivation, hypoxia, reactive oxygen species, DNA damage, protein aggregates, damaged organelles, or intracellular pathogens. Both specific, stimulus-dependent and more general, stimulus-independent signaling pathways are activated to coordinate different phases of autophagy. Autophagy can be integrated with other cellular stress responses through parallel stimulation of autophagy and other stress responses by specific stress stimuli, through dual regulation of autophagy and other stress responses by multifunctional stress signaling molecules, and/or through mutual control of autophagy and other stress responses. Thus, autophagy is a cell biological process that is a central component of the integrated stress response.
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