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Background
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The ABL1 protooncogene encodes 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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- Donaldson, L.W., et al., Proc. Natl. Acad. Sci. U.S.A. 99(22):14053-14058 (2002).
- Pisabarro, M.T., et al., J. Mol. Biol. 281(3):513-521 (1998).
- Nam, H.J., et al., Structure 4(9):1105-1114 (1996).
- Chissoe, S.L., et al., Genomics 27(1):67-82 (1995).
- Gosser, Y.Q., et al., Structure 3(10):1075-1086 (1995).
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