The fusion protein BCRABL results in constitutive tyrosine kinase activity. It also affects downstream targets as well as the subcellular location of the normally tightly regulated Abl tyrosine kinase.
Methods
The authors review the current knowledge concerning the signaling networks associated with BCRABL–dependent transformation.
Results
Although BCRABL is considered a single genetic change, the dysregulated tyrosine kinase activates a network of signals that contributes to cytokine-independent growth, resistance to apoptosis, and genetic instability.
Conclusions
The effectiveness of BCRABL–dependent transformation of hematopoietic stem cells is due not to a single pathway but rather to the culmination of a network of signaling pathways.
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