Document Detail


Autophagy in cellular growth control.
MedLine Citation:
PMID:  20096689     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cell growth is regulated by two antagonistic processes: TOR signaling and autophagy. These processes integrate signals including growth factors, amino acids, and energy status to ensure that cell growth is appropriate to environmental conditions. Autophagy responds indirectly to the cellular milieu as a downstream inhibitory target of TOR signaling and is also directly controlled by nutrient availability, cellular energy status, and cell stress. The control of cell growth by TOR signaling and autophagy are relevant to disease, as altered regulation of either pathway results in tumorigenesis. Here we give an overview of how TOR signaling and autophagy integrate nutritional status to regulate cell growth, how these pathways are coordinately regulated, and how dysfunction of this regulation might result in tumorigenesis.
Authors:
Richard C Wang; Beth Levine
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2010-01-22
Journal Detail:
Title:  FEBS letters     Volume:  584     ISSN:  1873-3468     ISO Abbreviation:  FEBS Lett.     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-03-22     Completed Date:  2010-04-09     Revised Date:  2014-09-12    
Medline Journal Info:
Nlm Unique ID:  0155157     Medline TA:  FEBS Lett     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1417-26     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animals
Autophagy*
Cell Cycle
Cell Proliferation
Energy Metabolism
Humans
Neoplasms / pathology
Signal Transduction
Grant Support
ID/Acronym/Agency:
K08 CA164047/CA/NCI NIH HHS; R01 CA084254/CA/NCI NIH HHS; R01 CA084254-10/CA/NCI NIH HHS; R01 CA084254-10S1/CA/NCI NIH HHS; R01 CA109618/CA/NCI NIH HHS; R01 CA109618/CA/NCI NIH HHS; R01 CA109618-05/CA/NCI NIH HHS; R01 CA84254/CA/NCI NIH HHS
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