Activation of AMPK and inactivation of Akt result in suppression of mTOR-mediated S6K1 and 4E-BP1 pathways leading to neuronal cell death in in vitro models of Parkinson's disease

Cellular Signalling

Volumn 26, Issue 8, 2014, Pages 1680-1689

  Xu, Yijiao ^a   Liu, Chunxiao ^a   Chen, Sujuan ^a   Ye, Yangjing ^a   Guo, Min ^a   Ren, Qian ^a   Liu, Lei ^b   Zhang, Hai ^a   Xu, Chong ^a   Zhou, Qian ^a   Huang, Shile ^b   Chen, Long ^a  

^a NANJING NORMAL UNIVERSITY   (China)

^b LOUISIANA STATE UNIVERSITY HEALTH SCIENCES CENTER   (United States)

Author keywords

Akt; AMPK; MTOR; Neuronal cells; Parkinson's disease

Indexed keywords

1 METHYL 4 PHENYLPYRIDINIUM; CASPASE 3; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE KINASE; INITIATION FACTOR 4E BINDING PROTEIN 1; MAMMALIAN TARGET OF RAPAMYCIN; NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE; OXIDOPAMINE; PROTEIN KINASE B; ROTENONE; S6K1 PROTEIN; UNCLASSIFIED DRUG; CARRIER PROTEIN; EIF4EBP1 PROTEIN, RAT; PHOSPHOPROTEIN; S6 KINASE; S6K1 PROTEIN, RAT; TARGET OF RAPAMYCIN KINASE;

ANIMAL CELL; ARTICLE; CELL DEATH; CELL VIABILITY; CONTROLLED STUDY; DOWN REGULATION; ENZYME ACTIVATION; ENZYME INACTIVATION; ENZYME PHOSPHORYLATION; FETUS; GENE OVEREXPRESSION; MOUSE; NERVE CELL; NONHUMAN; PARKINSON DISEASE; PRIORITY JOURNAL; RAT; ANIMAL; ANTAGONISTS AND INHIBITORS; APOPTOSIS; BIOLOGICAL MODEL; CELL CULTURE; CELL SURVIVAL; CYTOLOGY; DRUG EFFECTS; GENETICS; METABOLISM; PATHOLOGY; PC12 CELL LINE; PHOSPHORYLATION; SIGNAL TRANSDUCTION; TOXICITY;

1-METHYL-4-PHENYLPYRIDINIUM; AMP-ACTIVATED PROTEIN KINASES; ANIMALS; APOPTOSIS; CARRIER PROTEINS; CASPASE 3; CELL SURVIVAL; CELLS, CULTURED; MODELS, BIOLOGICAL; NEURONS; OXIDOPAMINE; PARKINSON DISEASE; PC12 CELLS; PHOSPHOPROTEINS; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-AKT; RATS; RIBOSOMAL PROTEIN S6 KINASES; ROTENONE; SIGNAL TRANSDUCTION; TOR SERINE-THREONINE KINASES;

EID: 84899984684     PISSN: 08986568     EISSN: 18733913     Source Type: Journal    
DOI: 10.1016/j.cellsig.2014.04.009     Document Type: Article

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