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Background
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ABL1 is a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell differentiation, cell division, cell adhesion, and stress response. Activity of c-Abl protein is negatively regulated by its SH3 domain, and deletion of the SH3 domain turns ABL1 into an oncogene. The t(9;22) translocation results in the head-to-tail fusion of the BCR and ABL1 genes present in many cases of chronic myelogeneous leukemia. The DNA-binding activity of the ubiquitously expressed ABL1 tyrosine kinase is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function for ABL1.
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Background
References
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- Barnes, K., et al., Oncogene 24(20):3257-3267 (2005).
- Kim, Y.R., et al., Genes Chromosomes Cancer 43(1):37-44 (2005).
- Aichberger, K.J., et al., Blood 105(8):3303-3311 (2005).
- Wei, G., et al., J. Biol. Chem. 280(13):12271-12278 (2005).
- Robinson, H.M., et al., Leukemia 19(4):564-571 (2005).
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