abl an oncogene from murine Abelson leukemia virus. The human equivalent is ABL (locus at 9q34), which encodes a tyrosine protein kinase. In humans, inappropriate activation of ABL occurs via a reciprocal translocation between chromosomes 9 and 22 in which ABL is joined at the breakpoint cluster region (bcr) of the ph1 gene on chromosome 22(q11), resulting in an altered chromosome 22, referred to as the Philadelphia chromosome (Ph1 ). The protein product of the spliced genes in the Ph1 chromosome is a molecule of 210 kDa, which has increased tyrosine kinase activity. The Ph1 chromosome occurs in most patients with chronic myelogenous leukemia. c-Abl can potentially regulate cell growth and may participate in growth regulation at multiple cellular locations, interacting with different cell components. It contains SH2 and SH3 domains (see SH domains) and also domains involved in binding to F-actin and DNA, and occurs in both cytoplasmic and nuclear locations. Its DNA-binding activity appears to be cell-cycle-regulated by Cdc2- mediated phosphorylation; it binds the retinoblastoma protein indicating involvement in transcriptional regulation.



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