Hypo- and hyperactivated Notch signaling induce a glycolytic switch through distinct mechanisms

Proceedings of the National Academy of Sciences of the United States of America

Volumn 108, Issue 46, 2011, Pages 18814-18819

  Landor, Sebastian K J ^a,b   Mutvei, Anders P ^b   Mamaeva, Veronika ^a   Jin, Shaobo ^b   Busk, Morten ^c   Borra, Ronald ^a,d   Grönroos, Tove J ^a   Kronqvist, Pauliina ^a   Lendahl, Urban ^b   Sahlgren, Cecilia Maria ^a  

^a UNIVERSITY OF TURKU   (Finland)

^b KAROLINSKA INSTITUTE   (Sweden)

^c AARHUS UNIVERSITY HOSPITAL   (Denmark)

^d TURKU UNIVERSITY HOSPITAL   (Finland)

Author keywords

[No Author keywords available]

Indexed keywords

NOTCH RECEPTOR; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN P53; PROTEIN SERINE KINASE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BREAST TUMOR; CANCER CELL; CELL ENERGY; CELL METABOLISM; CONTROLLED STUDY; GLYCOLYSIS; HUMAN; HUMAN CELL; MOLECULAR MECHANICS; MOUSE; NONHUMAN; OXIDATIVE PHOSPHORYLATION; PHENOTYPE; PRIORITY JOURNAL; TUMOR GROWTH; XENOGRAFT;

ANIMALS; GENE EXPRESSION REGULATION, NEOPLASTIC; GLYCOLYSIS; HOMEOSTASIS; HUMANS; MICE; MITOCHONDRIA; MODELS, BIOLOGICAL; NEOPLASM TRANSPLANTATION; OXIDATIVE PHOSPHORYLATION; OXYGEN; PHOSPHATIDYLINOSITOL 3-KINASES; PHOSPHORYLATION; RECEPTORS, NOTCH; SIGNAL TRANSDUCTION; TUMOR SUPPRESSOR PROTEIN P53;

EID: 81755163576     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.1104943108     Document Type: Article

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