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The ABL tyrosine kinase, encoded by the *ABL1* gene, is a nonreceptor tyrosine kinase involved in a wide range of cellular processes, including cell proliferation, differentiation, survival, migration, and DNA repair. Its activity is tightly regulated by intramolecular interactions and phosphorylation. Dysregulation, often through chromosomal translocations like t(9;22) leading to the BCR-ABL fusion protein, is a key driver of hematopoietic malignancies such as chronic myelogenous leukemia (CML). Targeting ABL has proven clinically successful, with drugs like imatinib inhibiting aberrant Abl-family kinases.
The Abl kinase transfers γ-phosphate from ATP onto specific tyrosines on substrate proteins/peptides. This phosphorylation event alters target protein function—affecting their activity state, cellular location, or interaction networks—which underlies its broad impact on cell fate decisions.
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