Indirect effects of Bax and Bak initiate the mitochondrial alterations that lead to cytochrome c release during arsenic trioxide-induced apoptosis.

@article{Nutt2005IndirectEO,
  title={Indirect effects of Bax and Bak initiate the mitochondrial alterations that lead to cytochrome c release during arsenic trioxide-induced apoptosis.},
  author={Leta K. Nutt and Vladimir Gogvadze and Wanlaya Uthaisang and Banafsheh Mirnikjoo and David James McConkey and Sten Orrenius},
  journal={Cancer biology & therapy},
  year={2005},
  volume={4 4},
  pages={459-67}
}
Arsenic trioxide is a potent chemotherapeutic agent by virtue of its ability to selectively trigger apoptosis in tumor cells. Previous studies have demonstrated that arsenicals cause direct damage to mitochondria, but it is not clear that these effects initiate apoptosis. Here we used Bak-/- mouse liver mitochondria and virally immortalized Bax-/- Bak-/- mouse embryonic fibroblasts (MEFs) to investigate whether or not multidomain proapoptotic BCL-2 family proteins were required for arsenic… CONTINUE READING

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