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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 (MIM:151410) 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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- Saglio, G., et al., Cell. Mol. Life Sci. 61(23):2897-2911 (2004).
- Deming, P.B., et al., Mol. Cell. Biol. 24(23):10289-10299 (2004).
- Graux, C., et al., Nat. Genet. 36(10):1084-1089 (2004).
- Monma, F., et al., Int. J. Hematol. 80(2):155-158 (2004).
- Gustafson, W.C., et al., J. Biol. Chem. 279(10):9400-9408 (2004).
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