Overexpression of Bcl-X(L) inhibits Ara-C-induced mitochondrial loss of cytochrome c and other perturbations that activate the molecular cascade of apoptosis.

@article{Kim1997OverexpressionOB,
  title={Overexpression of Bcl-X(L) inhibits Ara-C-induced mitochondrial loss of cytochrome c and other perturbations that activate the molecular cascade of apoptosis.},
  author={Caryn Naekyung Kim and Xiaofei Wang and Yinyin Huang and Ana Maria Ibrado and Leyuan Liu and Guofu Fang and K N Bhalla},
  journal={Cancer research},
  year={1997},
  volume={57 15},
  pages={3115-20}
}
High-dose Ara-C (HIDAC) induces the cleavage and activity of caspase-3 (CPP32beta/Yama/apopain), resulting in the morphological and biochemical features of apoptosis. High levels of the antiapoptotic Bcl-x(L) or Bcl-2, relative to the proapoptotic Bax, have been shown to inhibit HIDAC-induced cleavage and activity of caspase-3 and apoptosis of the human acute myeloid leukemia HL-60 cells. In a previous report, we demonstrated this inhibition, using the control HL-60 (HL-60/neo) cells and their… CONTINUE READING
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The release of cytochromec frommitochondria : a primarysite for Bcl - 2 regulationof apoptosis

  • P. L. Simonian, D. A. M. Grillot, D. W. Andrews, B. Leber, G. Nuà ± ez
  • Science ( Washington DC )
  • 1997

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