Pro-apoptotic effect of the c-Abl tyrosine kinase in the cellular response to 1-β-D-arabinofuranosylcytosine (original) (raw)

Oncogene volume 15, pages 1947–1952 (1997)Cite this article

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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Authors and Affiliations

  1. Division of Cancer Pharmacology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, 02115, Massachusetts, USA
    Yinyin Huang, Zhi-Min Yuan, Takatoshi Ishiko, Shuji Nakada, Taiju Utsugisawa, Tomohisa Kato, Surender Kharbanda & Donald W Kufe

Authors

  1. Yinyin Huang
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  2. Zhi-Min Yuan
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  3. Takatoshi Ishiko
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  4. Shuji Nakada
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  5. Taiju Utsugisawa
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  6. Tomohisa Kato
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  7. Surender Kharbanda
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  8. Donald W Kufe
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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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