boc-Aspartyl(OMe)-fluoromethylketone attenuates mitochondrial release of cytochrome c and delays brain tissue loss after traumatic brain injury in rats.

@article{Clark2007bocAspartylOMefluoromethylketoneAM,
  title={boc-Aspartyl(OMe)-fluoromethylketone attenuates mitochondrial release of cytochrome c and delays brain tissue loss after traumatic brain injury in rats.},
  author={Robert B. Clark and Paula D. Nathaniel and Xiaopeng Zhang and Clifton Edward Dixon and Sean M. Alber and Simon C Watkins and John A. Melick and Patrick M Kochanek and Steven H Graham},
  journal={Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism},
  year={2007},
  volume={27 2},
  pages={
          316-26
        }
}
The pathobiology of traumatic brain injury (TBI) includes activation of multiple caspases followed by cell death with a spectrum of apoptotic phenotypes. There are initiator (e.g. caspase-2, -8, and -9) and effector (e.g. caspase-3 and -7) caspases. Recently, caspase-2 and -8 have been shown to regulate cell death via provoking cytochrome c release from the mitochondria upstream of caspase-9. Here, we show that an intracerebral injection of the pan-caspase inhibitor boc-Aspartyl(OMe… CONTINUE READING
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