Document Detail

Alkaline stress-induced autophagy is mediated by mTORC1 inactivation.
MedLine Citation:
PMID:  21590709     Owner:  NLM     Status:  MEDLINE    
The activation of autophagic pathway by alkaline stress was investigated. Various types of mammalian cells were subjected to alkaline stress by incubation in bicarbonate buffered media in humidified air containing atmospheric 0.04% CO(2) . The induction of autophagy following alkaline stress was evaluated by assessing the conversion of cytosolic LC3-I into lipidated LC3-II, the accumulation of autophagosomes, and the formation of autolysosomes. Colocalization of GFP-LC3 with endolysosomal marker in HeLa GFP-LC3 cells undergoing autophagic process by alkaline stress further demonstrates that autophagosomes triggered by alkaline stress matures into autolysosomes for the lysosome dependent degradation. We found that the inactivation of mTORC1 is important for the pathway leading to the induction of autophagy by alkaline stress since the expression of RhebQ64L, a constitutive activator of mTORC1, downregulates the induction of autophagy after alkaline stress in transfected human 293T cells. These results imply that activation of autophagic pathway following the inactivation of mTORC1 is important cellular events governing alkaline stress-induced cytotoxicity and clinical symptoms associated with alkalosis.
Jinkyu Suk; Sang Su Kwak; Jae Ho Lee; Ji Hye Choi; Sang-Hee Lee; Dong Hwan Lee; Boohyeong Byun; Geon-Hyoung Lee; Cheol O Joe
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular biochemistry     Volume:  112     ISSN:  1097-4644     ISO Abbreviation:  J. Cell. Biochem.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-08-19     Completed Date:  2011-12-07     Revised Date:  2013-09-30    
Medline Journal Info:
Nlm Unique ID:  8205768     Medline TA:  J Cell Biochem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2566-73     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Wiley-Liss, Inc.
Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, South Korea.
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MeSH Terms
Alkalosis / metabolism,  physiopathology*
Cell Size
Enzyme Activation
HEK293 Cells
HeLa Cells
Lysosomes / metabolism
Microtubule-Associated Proteins / metabolism
Monomeric GTP-Binding Proteins / genetics,  metabolism
Mutation, Missense
Neuropeptides / genetics,  metabolism
Phagosomes / metabolism
Proteins / metabolism*
Proto-Oncogene Proteins c-akt / metabolism
Recombinant Fusion Proteins / genetics,  metabolism
Signal Transduction
Stress, Physiological*
Reg. No./Substance:
0/Microtubule-Associated Proteins; 0/Neuropeptides; 0/Proteins; 0/RHEB protein, human; 0/Recombinant Fusion Proteins; 0/light chain 3, human; 0/mechanistic target of rapamycin complex 1; EC Proteins c-akt; EC GTP-Binding Proteins

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