The two major imatinib resistance mutations E255K and T315I enhance the activity of BCR/ABL fusion kinase

Biochemical and Biophysical Research Communications

Volumn 319, Issue 4, 2004, Pages 1272-1275

  Yamamoto, Masahide ^a   Kurosu, Tetsuya ^a   Kakihana, Kazuhiko ^a   Mizuchi, Daisuke ^a   Miura, Osamu ^a  

^a TOKYO MEDICAL AND DENTAL UNIVERSITY   (Japan)

Author keywords

BCR ABL; Chronic myeloid leukemia; Imatinib; Mutation; Tyrosine kinase

Indexed keywords

BCR ABL PROTEIN; CELL PROTEIN; IMATINIB; PHOSPHOTRANSFERASE; STAT5 PROTEIN;

ANIMAL CELL; ARTICLE; AUTOPHOSPHORYLATION; CELL STRAIN COS7; CONTROLLED STUDY; ENZYME ACTIVITY; ENZYME ANALYSIS; ENZYME ASSAY; IN VITRO STUDY; MUTATION; NONHUMAN; NUCLEOTIDE SEQUENCE; PRIORITY JOURNAL; PROTEIN ANALYSIS; PROTEIN DOMAIN; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION;

ANIMALS; ANTINEOPLASTIC AGENTS; CERCOPITHECUS AETHIOPS; COS CELLS; DNA-BINDING PROTEINS; DRUG RESISTANCE, NEOPLASM; ENZYME INHIBITORS; FUSION PROTEINS, BCR-ABL; GLUTAMIC ACID; HUMANS; LEUKEMIA; MILK PROTEINS; MUTATION; PHOSPHORYLATION; PIPERAZINES; PROTEIN STRUCTURE, TERTIARY; PYRIMIDINES; STAT5 TRANSCRIPTION FACTOR; THREONINE; TRANS-ACTIVATORS;

EID: 2942573506     PISSN: 0006291X     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.bbrc.2004.05.113     Document Type: Article

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