Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent ATP-based oncogenic protein kinase inhibitor: implications for CML. [electronic resource]
Producer: 20041123Description: 2532-9 p. digitalISSN:- 0006-4971
- Adaptor Proteins, Signal Transducing -- metabolism
- Adenosine Triphosphate -- analogs & derivatives
- Amino Acids -- genetics
- Apoptosis -- drug effects
- Benzamides
- Cell Cycle -- drug effects
- Cell Division -- drug effects
- DNA-Binding Proteins -- metabolism
- Enzyme Inhibitors -- chemistry
- Fusion Proteins, bcr-abl -- antagonists & inhibitors
- Gene Expression Regulation, Neoplastic
- HL-60 Cells
- Humans
- Imatinib Mesylate
- Inhibitory Concentration 50
- K562 Cells
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive -- enzymology
- Milk Proteins -- metabolism
- Models, Molecular
- Mutation -- genetics
- Nuclear Proteins -- metabolism
- Phosphorylation -- drug effects
- Phosphotyrosine -- metabolism
- Piperazines -- chemistry
- Protein Structure, Tertiary
- Pyridones -- chemistry
- Pyrimidines -- chemistry
- STAT5 Transcription Factor
- Trans-Activators -- metabolism
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
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