Regulation of the c-Abl and Bcr-Abl Tyrosine Kinases

Nat Rev Mol Cell Biol. 2004 Jan;5(1):33-44. doi: 10.1038/nrm1280.

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

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Binding Sites
  • CSK Tyrosine-Protein Kinase
  • Catalysis
  • Fusion Proteins, bcr-abl / genetics*
  • Fusion Proteins, bcr-abl / metabolism*
  • Gene Expression Regulation / genetics*
  • Humans
  • Leukemia / genetics
  • Molecular Sequence Data
  • Phosphorylation
  • Point Mutation
  • Protein Conformation
  • Protein-Tyrosine Kinases / chemistry
  • Protein-Tyrosine Kinases / genetics
  • Protein-Tyrosine Kinases / metabolism
  • Proto-Oncogene Proteins c-abl / chemistry
  • Proto-Oncogene Proteins c-abl / genetics*
  • Proto-Oncogene Proteins c-abl / metabolism*
  • Sequence Alignment
  • Sequence Homology, Amino Acid
  • src Homology Domains
  • src-Family Kinases

Substances

  • Protein-Tyrosine Kinases
  • CSK Tyrosine-Protein Kinase
  • Fusion Proteins, bcr-abl
  • Proto-Oncogene Proteins c-abl
  • src-Family Kinases
  • CSK protein, human