Heat shock protein 60 or 70 activates nitric-oxide synthase (NOS) I- and inhibits NOS II-associated signaling and depresses the mitochondrial apoptotic cascade during brain stem death.

@article{Chan2007HeatSP,
  title={Heat shock protein 60 or 70 activates nitric-oxide synthase (NOS) I- and inhibits NOS II-associated signaling and depresses the mitochondrial apoptotic cascade during brain stem death.},
  author={Julie Y. H. Chan and Hsiao-Lei Cheng and Jimmy Li-Jer Chou and Faith C. H. Li and Kuang-Yu Dai and Samuel H. H. Chan and Alice Y. W. Chang},
  journal={The Journal of biological chemistry},
  year={2007},
  volume={282 7},
  pages={4585-600}
}
The cellular and molecular basis of brain stem death remains an enigma. As the origin of a "life-and-death" signal that reflects the progression toward brain stem death, the rostral ventrolateral medulla (RVLM) is a suitable neural substrate for mechanistic delineation of this phenomenon. Here, we evaluated the hypothesis that heat shock proteins (HSPs) play a neuroprotective role in the RVLM during brain stem death and delineated the underlying mechanisms, using a clinically relevant animal… CONTINUE READING