Differential complementation of Bcr-Abl point mutants with c-Myc Academic Article uri icon


MeSH Major

  • Adaptor Proteins, Signal Transducing
  • Cell Transformation, Neoplastic
  • Fusion Proteins, bcr-abl
  • Genes, abl
  • Genes, myc


  • A complementation strategy was developed to define the signaling pathways activated by the Bcr-Abl tyrosine kinase. Transformation inactive point mutants of Bcr-Abl were tested for complementation with c-Myc. Single point mutations in the Src-homology 2 (SH2) domain, the major tyrosine autophosphorylation site of the kinase domain, and the Grb-2 binding site in the Bcr region impaired the transformation of fibroblasts by Bcr-Abl. Hyperexpression of c-Myc efficiently restored transformation activity only to the Bcr-Abl SH2 mutant. These data support a model in which Bcr-Abl activates at least two independent pathways for transformation. This strategy may be useful for discerning signaling pathways activated by other oncogenes.

publication date

  • April 15, 1994



  • Academic Article



  • eng

PubMed ID

  • 8153630

Additional Document Info

start page

  • 424

end page

  • 6


  • 264


  • 5157