| Connecting autophagy to senescence in pathophysiology. | |
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MedLine Citation:
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PMID: 20045302 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cellular senescence is an extremely stable form of cell cycle arrest activated in response to stress. Autophagy, a lysosome-dependent cellular catabolic process, can also be triggered by cellular stresses. Both senescence and autophagy have been implicated in a similar range of pathophysiologies, including cancer, aging and age-related symptoms. Senescence is a heterogeneous phenotype that is composed of multiple effector mechanisms and autophagy was recently identified as a new effector of senescence. Autophagy seemingly has different impacts on cells responding to stress through a diversity of effects: recycling of metabolic waste, cell survival and protein expression regulation. |
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Authors:
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Andrew Rj Young; Masashi Narita |
Publication Detail:
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Type: Journal Article Date: 2010-01-04 |
Journal Detail:
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Title: Current opinion in cell biology Volume: 22 ISSN: 1879-0410 ISO Abbreviation: Curr. Opin. Cell Biol. Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-04-12 Completed Date: 2010-06-23 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8913428 Medline TA: Curr Opin Cell Biol Country: England |
Other Details:
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Languages: eng Pagination: 234-40 Citation Subset: IM |
Copyright Information:
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Copyright 2009 Elsevier Ltd. All rights reserved. |
Affiliation:
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Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Cambridge, CB2 0RE, United Kingdom. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Autophagy* Cell Aging* Disease* Feedback, Physiological Humans Intracellular Signaling Peptides and Proteins / metabolism Phenotype Protein-Serine-Threonine Kinases / metabolism beta-Galactosidase / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Intracellular Signaling Peptides and Proteins; EC 2.7.1.-/mTOR protein; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 3.2.1.23/beta-Galactosidase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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