Differential Complementation of Bcr-Abl Point Mutants with c-Myc
- 15 April 1994
- journal article
- other
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 264 (5157), 424-426
- https://doi.org/10.1126/science.8153630
Abstract
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.This publication has 25 references indexed in Scilit:
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