Abstract
The prototypic non-receptor tyrosine kinase c-Abl is implicated in various cellular processes. Its oncogenic counterpart, the Bcr-Abl fusion protein, causes certain human leukaemias. Recent insights into the structure and regulation of the c-Abl and Bcr-Abl tyrosine kinases have changed the way we look at these enzymes.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Amino Acid Sequence
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Animals
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Binding Sites
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CSK Tyrosine-Protein Kinase
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Catalysis
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Fusion Proteins, bcr-abl / genetics*
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Fusion Proteins, bcr-abl / metabolism*
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Gene Expression Regulation / genetics*
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Humans
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Leukemia / genetics
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Molecular Sequence Data
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Phosphorylation
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Point Mutation
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Protein Conformation
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Protein-Tyrosine Kinases / chemistry
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Protein-Tyrosine Kinases / genetics
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Protein-Tyrosine Kinases / metabolism
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Proto-Oncogene Proteins c-abl / chemistry
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Proto-Oncogene Proteins c-abl / genetics*
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Proto-Oncogene Proteins c-abl / metabolism*
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Sequence Alignment
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Sequence Homology, Amino Acid
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src Homology Domains
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src-Family Kinases
Substances
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Protein-Tyrosine Kinases
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CSK Tyrosine-Protein Kinase
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Fusion Proteins, bcr-abl
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Proto-Oncogene Proteins c-abl
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src-Family Kinases
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CSK protein, human