Article
Alternative signals to RAS for hematopoietic transformation by the BCR-ABL oncogene.
Cell - 22 Sept 1995
Goga A, McLaughlin J, Afar D E, Saffran D C, Witte O N
Abstract excerpt
Biological function of the BCR-ABL oncogene is dependent on its activated tyrosine kinase. Mutations that inactivate the SRC homology 2 (SH2) domain, the GRB2-binding site in BCR, or the major autophosphorylation site of the kinase domain selectively disrupt downstream signaling but not tyrosine kinase activity. Despite a loss of fibroblast transformation activity, all three mutants retain the ability to render...
Topics
- Animals
- Bone Marrow Cells
- Cell Line, Transformed
- Cell Transformation, Neoplastic
- Fibroblasts
- Fusion Proteins, bcr-abl
- Granulocytes
- Hematopoietic Cell Growth Factors
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive
- Lymphocytes