Differential signaling by alternative HGF isoforms through c-Met: Activation of both MAP kinase and PI 3-kinase pathways is insufficient for mitogenesis

Oncogene

Volumn 18, Issue 22, 1999, Pages 3399-3406

  Day, Regina M ^a   Cioce, Vittoria ^b   Breckenridge, Diane ^a   Castagnino, Paola ^a   Bottaro, Donald P ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

^b NATIONAL HEART LUNG AND BLOOD INSTITUTE   (United States)

Author keywords

c Met; HGF; MAPK; Mitogenesis; Motogenesis; PI 3 kinase

Indexed keywords

2 (2 AMINO 3 METHOXYPHENYL)CHROMONE; MITOGEN ACTIVATED PROTEIN KINASE; PHOSPHATIDYLINOSITOL 3 KINASE; SCATTER FACTOR; SCATTER FACTOR RECEPTOR; WORTMANNIN;

ARTICLE; AUTOPHOSPHORYLATION; BREAST EPITHELIUM; DNA SYNTHESIS; EPITHELIUM CELL; GENETIC TRANSFECTION; HUMAN; HUMAN CELL; MITOGENESIS; PRIORITY JOURNAL; SIGNAL TRANSDUCTION;

1-PHOSPHATIDYLINOSITOL 3-KINASE; ANIMALS; CA(2+)-CALMODULIN DEPENDENT PROTEIN KINASE; CELL LINE; CELL MOVEMENT; DNA; ENZYME ACTIVATION; EPITHELIAL CELLS; GENE EXPRESSION REGULATION; HEPATOCYTE GROWTH FACTOR; HUMANS; MICE; MITOGENS; PHOSPHORYLATION; PROTEIN ISOFORMS; PROTO-ONCOGENE PROTEINS C-MET; SIGNAL TRANSDUCTION; STEM CELLS; TRANSFECTION;

EID: 0033519718     PISSN: 09509232     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.onc.1202683     Document Type: Article

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