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v-Abl, encoded by the Abelson murine leukemia virus, is a non-receptor tyrosine kinase with potent oncogenic activity in mice (for review, see Refs. 1 and 2). A similar human oncoprotein, BCR-ABL, is critical in the pathogenesis of 95% of chronic myelogenous leukemia (CML)1and 10% of acute lymphocytic leukemia (for review, see Refs. 3 and 4). The c-Abl proto-oncoprotein was identified as the normal cellular homolog of v-Abl (for review, see Ref. 2). The increased tyrosine kinase activities of v-Abl and BCR-ABL, compared with the cellular c-Abl, correlate with their transforming activities.
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Zou et al. (1999) studied this question.
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