Activating mutations in the Met receptor overcome the requirement for autophosphorylation of tyrosines crucial for wild type signaling

Oncogene

Volumn 18, Issue 36, 1999, Pages 5120-5125

  Jeffers, Michael ^a,b   Vande Woude, George F ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

^b CURAGEN CORPORATION   (United States)

Author keywords

Autophosphorylation; Mutant Met; Signaling

Indexed keywords

PROTEIN TYROSINE KINASE; TYROSINE KINASE RECEPTOR;

ANIMAL CELL; ARTICLE; AUTOPHOSPHORYLATION; CANCER; CONTROLLED STUDY; ENZYME ACTIVITY; ENZYME CONFORMATION; GENE MUTATION; MOUSE; NONHUMAN; PRIORITY JOURNAL; SIGNAL TRANSDUCTION;

3T3 CELLS; ANIMALS; HUMANS; MICE; MUTATION; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-MET; RECEPTOR, NERVE GROWTH FACTOR; RECOMBINANT FUSION PROTEINS; SIGNAL TRANSDUCTION; TYROSINE;

ANIMALIA;

EID: 0033539042     PISSN: 09509232     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.onc.1202902     Document Type: Article

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