Abstract
Treatment of cells with the antimetabolite 1-β-D-arabinofuranosylcytosine (ara-C) and other genotoxic agents is associated with activation of the c-Abl protein tyrosine kinase. The functional role of c-Abl in the response to DNA damage, however, remains unclear. The present studies demonstrate that cells expressing a dominant negative, kinase-inactive c-Abl (K-R) are resistant to killing by ara-C. The expression of c-Abl (K-R) blocked ara-C-induced apoptosis by a mechanism that is at least in part independent of the p53 tumor suppressor. Cells null for c-Abl also exhibited resistance to induction of apoptosis. These findings provide support for a pro-apoptotic function of c-Abl in the response to certain genotoxic drugs.
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Huang, Y., Yuan, ZM., Ishiko, T. et al. Pro-apoptotic effect of the c-Abl tyrosine kinase in the cellular response to 1-β-D-arabinofuranosylcytosine. Oncogene 15, 1947–1952 (1997). https://doi.org/10.1038/sj.onc.1201376
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DOI: https://doi.org/10.1038/sj.onc.1201376
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