Akt is a direct target for myricetin to inhibit cell transformation

Molecular and Cellular Biochemistry

Volumn 332, Issue 1-2, 2009, Pages 33-41

  Kumamoto, Takuma ^a   Fujii, Makoto ^a   Hou, De Xing ^a  

^a KAGOSHIMA UNIVERSITY   (Japan)

Author keywords

Akt; Cell transformation; Modeling; Myricetin

Indexed keywords

ADENOSINE TRIPHOSPHATE; CYCLIN D1; FLAVONOL; MYRICETIN; PROTEIN KINASE B; PROTEIN KINASE B INHIBITOR; PROTEIN SERINE THREONINE KINASE; TRANSCRIPTION FACTOR AP 1;

ANIMAL CELL; APOPTOSIS; ARTICLE; BINDING ASSAY; BINDING SITE; CELL GROWTH; CELL PROLIFERATION; CELL TRANSFORMATION; CONTROLLED STUDY; DATA ANALYSIS; DRUG TARGETING; ENZYME INHIBITION; ENZYME PHOSPHORYLATION; EX VIVO STUDY; FRUIT; HYDROGEN BOND; IN VITRO STUDY; MOLECULAR MODEL; MOUSE; NONHUMAN; SIGNAL TRANSDUCTION; TRANSACTIVATION; VEGETABLE;

1-PHOSPHATIDYLINOSITOL 3-KINASE; ADENOSINE TRIPHOSPHATE; ANIMALS; CELL ADHESION; CELL TRANSFORMATION, NEOPLASTIC; CELLS, CULTURED; CYCLIN D1; ELECTROPHORETIC MOBILITY SHIFT ASSAY; EPIDERMIS; FLAVONOIDS; G0 PHASE; G2 PHASE; IMMUNOBLOTTING; IMMUNOPRECIPITATION; LUCIFERASES; MICE; MODELS, MOLECULAR; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-AKT; SIGNAL TRANSDUCTION; TISSUE PLASMINOGEN ACTIVATOR; TRANSCRIPTION FACTOR AP-1;

EID: 70450286260     PISSN: 03008177     EISSN: 15734919     Source Type: Journal    
DOI: 10.1007/s11010-009-0171-9     Document Type: Article

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