Rapamycin induces feedback activation of Akt signaling through an IGF-1R-dependent mechanism

Oncogene

Volumn 26, Issue 13, 2007, Pages 1932-1940

  Wan, X ^a,b   Harkavy, B ^a   Shen, N ^a   Grohar, P ^a   Helman, L J ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

^b NATIONAL INSTITUTES OF HEALTH   (United States)

Author keywords

Akt; IGF 1R; mTOR; Rapamycin; Rhabdomyosarcoma

Indexed keywords

1,4 DIAMINO 1,4 BIS(2 AMINOPHENYLTHIO) 2,3 DICYANOBUTADIENE; 2 MORPHOLINO 8 PHENYLCHROMONE; INSULIN RECEPTOR SUBSTRATE 1; MAMMALIAN TARGET OF RAPAMYCIN INHIBITOR; MONOCLONAL ANTIBODY; MONOCLONAL ANTIBODY 7C10; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE B; RAPAMYCIN; SMALL INTERFERING RNA; SOMATOMEDIN B; SOMATOMEDIN C RECEPTOR; TEMSIROLIMUS; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CANCER IMMUNOTHERAPY; CANCER INHIBITION; CELL SURVIVAL; CHO CELL; CONCENTRATION RESPONSE; CONTROLLED STUDY; DOWN REGULATION; DRUG MECHANISM; DRUG POTENTIATION; ENZYME ACTIVATION; ENZYME INHIBITION; ENZYME PHOSPHORYLATION; FEEDBACK SYSTEM; FEMALE; GENE OVEREXPRESSION; HUMAN; HUMAN CELL; MOUSE; MYOBLAST; NONHUMAN; PRIORITY JOURNAL; RHABDOMYOSARCOMA; RNA INTERFERENCE; SIGNAL TRANSDUCTION; TUMOR XENOGRAFT;

1-PHOSPHATIDYLINOSITOL 3-KINASE; ANIMALS; BASE SEQUENCE; CHO CELLS; CRICETINAE; CRICETULUS; DNA PRIMERS; ENZYME ACTIVATION; FEEDBACK, BIOCHEMICAL; MICE; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-AKT; RECEPTOR, IGF TYPE 1; RNA INTERFERENCE; SIGNAL TRANSDUCTION; SIROLIMUS;

CRICETULUS GRISEUS; MAMMALIA;

EID: 33947538050     PISSN: 09509232     EISSN: 14765594     Source Type: Journal    
DOI: 10.1038/sj.onc.1209990     Document Type: Article

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